Fluids and Electrolytes

Dr. Ali Asghar Taseer

Assistant professor
Paediatric unit-II
FMU / Allied Hospital Faisalabad
 What We Will Discuss
• Major electrolytes, too low, too high and what
to do
• Common fluid and electrolyte issues that we
see everyday in the PICU
• And of course lots multiple choice questions
 What We Will Not Discuss
• TPN
• Any tubules, glomeruli, or arterioles
• Ca binding proteins
• Na-K transporters
• Dialysis, apart from specific indications
 First - Na
• 90% extracellular
• Major determinant of extracellular osmolality
• Very important for CNS
• Large rapid changes can be life threatening
• Small changes are harmless but warn of other
processes
• Check electrolytes!
 Hyponatremia - causes
• Decreased Na – increased loses, AI, CSW,
diuretics, osmotic loses (DKA)
• Increased Na – free water retention exceeds
Na retention, CHF, cirrhosis, nephrotic
syndrome, renal failure
• Normal Na - SIADH
 Which of the following drugs is NOT
associated with SIADH
A. Vincristine
B. Haldol
C. Azithromycin
D. Ecstasy
E. SSRI

C. Azithromycin
Hyponatremia: Symptoms & Treatment
• Cellular swelling and cerebral edema
• Lethargy, N/V, cramps, confusions
• Seizures and coma <120 (acute)
• Chronically CNS cells compensate – rapid
correction - osmotic demyelination
• Treatment – 1st stop herniation/seizures
• 5-6 ml/kg 3% will raise Na 5mEq/L
• Chronic or acute with CNS sx – 0.5mEq/L/h
• Acute with no CNS sx – 0.7-1mEq/L/h
• MUST follow levels!
How many mEq of Na are in a L of 3% Saline

A. 513
B. 462
C. 300
D. A lot
E. Too much math

Answer A. Normal saline is 0.9% 154mEq/L. Divide by 9.

Add to 154 to get “1% saline”. Multiple by 3. Other
options include google. Note “normal saline” is actually
not.
 Hypernatremia: Causes
• Decreased Na – free water loses > Na loses,
diarrhea, iatrogenic from insufficient free
water, diuresis
• Normal Na – DI
• Increased Na – usually iatrogenic – 3% in TBI,
NaHCO3 during resuscitation, improperly
prepared infant formula
Hypernatremia: Symptoms & Treatment
• Increased osmolality, most issues in CNS
• Irritability, spasticity, N/V, seizures, coma and of
course death
• Decreased brain cell volume – tearing of vessels,
subcortical or subdural bleeds, vascular congestion,
CVT, demyelination
• Accumulation of idiogenic osm in CNS cells occurs
with time
• Rapid correction – brain edema
• Correct over 48 h no faster than 1 mEq/L/H
Your otherwise stable TBI patient is on
3% saline gtt. Na is 156. Labs show
non-gap metabolic acidosis. WTF?
A. Shock
B. Hyperchloremia
C. Hyperphosphatemia
D. New onset DKA
E. Salicylate abuse
Answer: B in setting of hyperchloremia, kidneys
waste bicarb to maintain electro-neutrality.
 Now, K +
• Mostly intracellular
• Hypokalemia is common, rarely fatal
• Hyperkalemia is uncommon and very bad
• Mostly K is managed by kidneys and GI tract
• Also affected by acid-base balance, insulin,
catecholamines, Mg and aldosterone
• Kidneys secrete K during alkalosis and resorb it
during acidosis
• Cells exchange K+ for H+ when acidosis is caused
by excess H+ therefore….
 Hyperkalemia seen with DKA is due to:
A. Inappropriate fluids in the peds ED and PICU
B. Insulin deficiency
C. Excess H+ ions
D. Organic acids
E. Everyone knows hyperkalemia with DKA isn’t really real, I
am SO much smarter than this question

Answer: B because the acidosis is caused by organic acids, not

H+ ions, K+ does not leave the cells to maintain
electroneutrality, it leaves because of insulin deficiency.
Simplified, of course.
 Hypokalemia: causes, symptoms &
treatment
• Beta-agonists, hyperaldosteronism, elevated renin,
diuretics, osmotic diuresis, GI loses, malnutrition, re-
feeding, geophagia, Barium poisoning, Barter
syndrome, RTA, drugs…
• Symptoms – flattened T-waves, ST depression, U-
waves, arrhythmias, weakness, ileus
• Treat – oral 1 mEq/kg or IV 0.5mEq/kg
• “Potential for catastrophic drug error in potassium
replacement is real.”
• Ask – does this K+ really need to be replaced?
 Hyperkalemia: Causes, symptoms &
Treatment
• Causes – redistribution, administration error, blood
products, rhabdo, hemolysis, renal failure, TLS,
metabolic acidosis, AI
• EKG – peaked T-waves, decreased P and R wave,
widened QRS, bradycardia, classic sine wave blending P
and QRS complex
• EKG can progress over minutes, CPA, V-fib/tach can
happen at any point in this progress
• < 6.5 remove K+ +/- kayexalate and monitor
• >6.5 or EKG changes, Ca+2 , insulin/glucose, sodium
bicarb, albuterol, dialysis, loop/thiazides diuretics
You are NF senior. A pt has a K+ of 7.5 with EKG
changes. What is the 1st thing you should do?
A. Order calcium
B. Order insulin/glucose
C. Order sodium bicarb
D. Call rapid response
E. Call code blue
F. Call PICU attending
Answer: Discuss. Real life is not multiple
choice….
Same patient has pulseless v-tach, the first
thing you should do?
A. CPR
B. Defibrillate
C. Calcium
D. Sodium bicarb
E. Insulin
F. Call a code blue
Answer: start (or make sure someone else starts)
CPR. Everything else should happen simultaneously,
again really life not multiple choice.
 Hypomagnesemia
• Mostly intracellular, muscle and bone
• Dietary deficiencies, malabsorption, renal dz
• Drugs – tacrolimus, cyclosporin, amphotercin,
cisplatin and diuretics
• Seizures, hypertension, ventricular
arrhythmias, coronary spasm and NM “stuff”
• Treat with Mg – 25-50 mg/kg watch for
respiratory depression and hypotension
 Hypermagnesemia
• Causes- iatrogenic and renal failure
• Symptoms – pseudocoma, hypotension and
respiratory depression, arrhythmias (theme),
decreased DTRs, eventually flaccid
quadriplegia
• Treatment – calcium (direct antagonist), lasix,
dialysis
You are the PICU fellow called to RRT for a 15 y/o
seizing, unresponsive, hypertensive small bowel
transplant patient. You treat the seizure, secure the
airway, transfer the patient and order labs. You expect…
A. High Mg, low tacrolimus
B. Low Mg, high tacrolimus
C. High Mg, high tacrolimus
D. Low Mg, low tacrolimus.

Answer: B. Both low Mg and high Tac will lower

seizure threshold and will also do so
synergistically.
 Hypophospatemia
• Mostly in bones, normal levels vary with age,
less is normal with age
• Symptoms only when < 1.5 – no ATP, 2,3-DPG
• Refeeding syndrome, burns, DKA, respiratory
alkolosis, and deficient TPN
• Symptoms – weakness, respiratory
depression, decreased O2 delievery
• Treat….with phos!
 Hyperphosphatemia
• Causes – TLS, renal failure, iatrogenic
• Symptoms – hypocalcemia, seizures, cardiac
arrest
• Treat – fluids, calcium, mannitol, dialysis
Anorexia, DKA, renal failure and new ALL can all
disturb phos, in which directions?
A. Re-feeding low phos, DKA high phos, renal failure
low phos, TLS high phos
B. Re-feeding high phos, DKA low phos, renal failure
high phos and TLS low phos
C. Re-feeding high phos, DKA high phos, renal failure
low phos and TLS high phos
D. Re-feeding low phos, DKA low phos, renal failure
high phos and TLS high phos
Answer: D. Note re-feeding syndrome and TLS are
opposite (K+ too). DKA pee out too much, renal failure
pee out not enough.
 Hypocalcemia
• Causes – reduced PTH, vitamin D, alkolosis,
hyperphos, drugs/toxins, TLS, blood products
(why?), the vague but common“critical illness”
• Symptoms – decreased muscle contractions,
stridor, apnea, tetany, seizures, muscle spasms,
hypotension, CHF, arrythmias, prolonged QT
• Treat – calcium. CaCl2 only via CVL, calcium
gluconate can go in PIV.
 Hypercalcemia
• Causes – hyper-PTH, vitamin D toxicity, malignancy,
immobility, thiazides
• Symptoms – hypertension, constipation, abdominal pain,
polyuria, dehydration, stones, hypotonia, shortened QT,
arrhythmias
• Remember stones, groans, bones and psychiatric moans
from Step 1?
• Treat – hydration, lasix, calcitonin (“tones” down calcium),
bisphosphonates
• Note – with calcium lasix and thiazides have opposite
effects.
 ICU FEN Issues: How Much?
• 4:2:1 rule generally applied
• Vented patients need less, don’t lose H 2O from
respiratory tract – 2/3 to 3/4 MIVF
• Rhabdomyolysis, DKA need more 1.5MIVF
• Shock, on-going loses – replace with boluses as needed
or else fluid overload can easily occur
• Septic shock should not be treated with 1.5 MIVF instead
of or even in addition to boluses, you risk fluid overload,
high Na, Cl and glucose and you won’t find this in ANY
septic shock algorithms, go ahead check your PALS card.
 ICU FEN issues: what?
• D5NS +/- KCl is safe go-to fluid
• Post-operative patients are at risk for
hyponatremia – should get NS
• Any neuro pt should absolutely get NS
• 1/2NS – small infants, DKA, borderline high Na
• 1/4NS – only with hypernatremia
 PICU FEN Issues – when to replace
electrolytes?
Probably let it be if some or all of Probably need to replace if ANY of
below is true below is true
• Stable patient • Symptomatic or critical
• Moderate deficiency (K or • Severely low levels (Mg is 1)
phos of 3.3) • NPO on IVF
• Eating patient • Expectation of on-going
• No expectation of on-going loses (giving more lasix)
loses • Deficit is consistent with
• Deficit not consistent with clinical situation
clinical picture - suggesting • Special cases – low Mg in
transient or spurious value transplants, low Na in TBI
 ICU fluid issues: what?
• TBI – no glucose for 72 h
• Everyone else D5
• Small infants or anyone at risk for
hypoglycemia, D10
 ICU FEN issues: checking labs
• Most ICU patients need lytes checked at or
near admission, especially critical patients,
asthmatics, DKA
• Who needs daily lytes? General guidelines…
• Anyone NPO/IVF
• Anyone on TPN that is being actively titrated
• Anyone on diuretics being actively titrated
• Anyone severely critical
PICU FEN Issues: My patient is not peeing…
fluids or lasix
Lasix Fluid
• No evidence of shock • Evidence of shock
• Good perfusion • Tachycardia
• Not tachycardic • Hypotension
• Normo/hypertensive • Dry mucus membranes,
• CVP > 6-8 sunken fontanelle
• BUN and Cr normal • Low CVP
• Suspicion of fluid overload • Elevated BUN
(wet CXR, edema) • Clinical explanation for fluid
• Clinical explanation for deficit (GI loses, OR)
urinary retention (PCA)
I am still not sure – insert foley