Fluids and Electrolytes Keith Torrey

Electrolytes (and fluids)
Intern Bootcamp
Department of Medicine
Keith Torrey, PGY-2, Internal Medicine-Pediatrics
Youre a new intern, new team
Patients are pretty stable on Monday
You started in a flurry of admittingLong, Medium. You make it to
Wednesday, short call, no overnights, just rounds for you!
You talk about Ms. Joneslooked fine, no Sx, exam unchanged, you
say electrolytes look fine at some point
Youre a new intern, new team
Patients are pretty stable on Monday
You started in a flurry of admittingLong, Medium. You make it to
Wednesday, short call, no overnights, just rounds for you!
You talk about Ms. Joneslooked fine, no Sx, exam unchanged, you
say electrolytes look fine at some point
The attending looks over at you and ask what you want to do about Ms.
Jones sodium of 128. She looks quizzical. (You hate quizzical)
The new senior looks back on the WoW; it was 137, 134, 130, etc
She was here for days, nothing in the HoT about this. Why didnt anybody DO
something about this? Where are the I/Os? Was she on fluids?? AHHH
Your MS-3 turns to you with starry eyed optimismhes new here
(Your AI rolls her eyestheyre studying for Step 2 so they know everything.)
The senior clears his throat but hes horrible at mouthing answers
So theres a reason for this
Fluid management is astoundingly common
How many hospitalized patients get a bolus or mIVF?
Ordering labs:
How many BMPs/RFPs/CMPs have you ordered?
(What IS an RFP??)
How much of this do you report?
(Or just Electrolytes look fine?)
Electrolyte disturbances: very common, can be dangerous!

Do you think about them well?
Do you hate this, kidneys, and me by association?
Objectives
Overall: How to think clinically about electrolytes:
Electrolytes:
1. Set the stage: what are we ordering?
Cost (literally) vs benefit (Patients vs academics vs habits)
2. Whats common? Why is that?
3. Whats dangerous? Why is that?
4. How to recognize an urgent problemNF or otherwise
5. Starters of how to puzzle through diagnosis/etiology
(HypoNa is not a diagnosisits a description, its a start)
6. How to correct well
Cost & contents of labs at UH
Test Contents Cost Worth it?
BMP Na/K/Cl/HCO3/BUN/Cr/Glu/Ca $206 Nope
CMP BMP + TProt, Alb, Alk Phos, AST/ALT, TBili $297 First shot, sure
RFP All of BMP + Phos, Alb $96 Yes
HFP TProt, Alb, Alk Phos, AST/ALT, TBili, DBili $193 If needed
Na $78 K $78 Cl $51 Phos $32 Mg $90 Ca (ionized) $140
http://www.uhhospitals.org/case/patients-and-visitors/billing-insurance-and-medical-records/patient-pricing-information
Cost & contents of labs at UH
For good measure:

POCT Glucose $32; Glucose Quant Blood $32
Blood culture $133
http://www.uhhospitals.org/case/patients-and-visitors/billing-insurance-and-medical-records/patient-pricing-information
Hospital Acquired Anemia & Daily Phlebotomy
A study in JAMA in 2011 evaluated hospital acquired anemia (in patients w/o
baseline anemia)
Moderate to severe HAA developed in 3551 patients (20%).
The mean (SD) phlebotomy volume was higher in patients with HAA (173.8
[139.3] mL) vs. those without HAA (83.5 [52.0 mL]; P < .001).
For every 50 mL of blood drawn, the risk of moderate to severe HAA

increased by 18% (relative risk [RR], 1.18; 95% confidence interval [CI],
1.13-1.22)
Each 1mL of blood drawn decreases hemoglobin by ~0.07 g/dL
(Paul Shaniuk is the greatest for contributing this slide)

Fluid Balance in the Body
Why is this chart always in these lectures?
Because this tiny corner

is where we act; all our
measurements and our
interventions will be
based off this
Fluid Compartments in the Body
2/3 ICF: Home of K, Phos, Mg, organelles, etc
1/3 ECF: This is overall diminished in Dehydration
75% of this is Interstitial
25% of this is IVF/Plasma (Its ~1/12 of TBW, ~5-8%)

15% arterial (1-2% of all TBW)
This is where we need fluids to help perfusion/shock
85% venous (5-7% of all TBW)
Measure everything here, infuse fluids here
Not reflective of the whole picture, is it?
Walk through the RFP
Where the electrolytes are found (Helps w/ Dx and Tx)
Hypo: Problems, recognition, diagnosis, correction
Hyper: Problems, recognition, diagnosis, correction

Pauls Case 1
55 year old male with no significant PMHx except for known chronic
alcoholism for 30 years (6 pack of beers daily and a 5th of vodka) who
presents with recurrent falls for the past 2 months.
No significant family, medical or social history except for alcoholism. Only

medication is celexa, started 2 months ago.
His daughter took him to the doctor where his vital signs were stable (HR
74 and BP 116/74), and got the following labs:
(Paul Shaniuk is the greatest for contributing this case)

Pauls Case 1
55 year old male with no significant PMHx except for known chronic
alcoholism for 30 years (6 pack of beers daily and a 5th of vodka)
who presents with recurrent falls for the past 2 months.
No significant family, medical or social history except for alcoholism.

Only medication is celexa, started 2 months ago.
His daughter took him to the doctor where his vital signs were
stable (HR 74 and BP 116/74), and got the following labs:
BMP 125/4.1/87/28/6/0.64<102. Negative CXR & UA.

He was admitted for further work-up.
Working Up Hyponatremia
1. Think about risks, time courseover weeks or over hours?
Based on History, whats your differential?
Differential Diagnosis?
Glucocorticoid Deficiency
Beer Potomania Hypothyroidism
SIADH Drug use
Cirrhosis Acute or Chronic Kidney failure
Pancreatitis Third spacing of fluids
Surreptitious Diuretic Use Type 2 RTA
Renal losses DKA
GI losses Osmotic diuresis
Chronic (2 months) and symptoms are possibly relatedsevere!
2. Volume status: Hypovolemic, Euvolemic, Hypervolemic?

Based on History & Physical
Hyponatremia: Causes 1/2
Hypovolemia
Extra-renal sodium loss (Una<10)
Sweat, diarrhea, vomiting
3rd spacing: trauma, burns, pancreatitis
Renal sodium loss (Una >20)
Diuretics
Mineralocorticoid deficiency
Cerebral salt wasting
Proximal type II RTA
Euvolemia (Una>20)
SIADH
Glucocorticoid deficiency
Hypothryoidism
Psychogenic polydipsia
Drugs: desmopressin, psychoactive agents, chemotx
Hyponatremia: Causes 2/2
Hypervolemia (Una<20)
Acute or chronic renal failure Una>20
Congestive heart failure
Cirrhosis/hepatic failure
Nephrotic syndrome
Hyperosmolar
Hyperglycemia, mannitol, glycine
Case Continued, Na 125
Physical exam showed a pale man who was A&Ox3 and in no
distress. Normal cardiac, respiratory and abdominal exam. JVP not
elevated
Neurologic exam showed b/l nystagmus with lateral gaze and

impaired b/l propioception in the lower extremities
Skin exam with normal turgor and multiple ecchymoses on his body.

Euvolemic based on physical exam
3. Think about Serum Osm and its components

Hypertonic is rare: too much Glu, Mannitol, Ureastop here
Hypotonic most commonfree water overpowers Na keep thinking
4. Is the body responding appropriately or inappropriately?

Based on Urine Osm, Urine Electrolytes
Sodium: Hyponatremia
Any other labs???
Serum osmolarity 254
Urine osmolarity 600
Urine sodium - 166


Euvolemic based on physical exam
3. Think about Serum Osm and its components

Serum Osm: 2(Na) + (BUN/2.8) + (Glu/18)
Not hypertonic by calc258nor by measurement
Measured Serum Osm is truly low how should the body adapt?

High Urine Osm, Na means body is dumping salt or resorbing water
Points to renal losses by renal failure or inappropriate actions on kidney
Case Conclusion
The patient was diagnosed with SIADH, most likely deemed to be
due to his celexa.
Picture was clouded by the fact that he was presumed to have

baseline hyponatremia due to alcohol use, but clinical picture did
not fit beer potomania (Urine Osm/Na would be low)
Patient improved with 1.5 L a day fluid restriction & holding celexa
Hyponatremia: Clinical signs & symptoms
Nausea/vomiting
Lethargy
Headache
Confusion
Seizures
Non-cardiogenic pulmonary edema
These are mostly due to CNS dysfunction and cerebral
edema!
Hyponatremia: Therapy
Acute change: Can correct quickly
Chronic change: Need to correct slowly

Risk of Central pontine myelinolysis
May be irreversible
Dysarthria, dysphagia, spastic paresis, coma
Check frequent sodiums (q1 or q2h)

Hyponatremia: Therapy
Can correct rapidly w/ 3% NS in severe symptomatic

patients (to level Na>120)
Normalize sodium at a rate of 8-12 mEq/L per 24h

Use NS almost alwaysrarely NS if youre removing underlying cause
Rise in [Na]/L = ([Na](solution) [Na](serum)) / (TBW+1)
Check frequent sodiums (q1 or q2h)

Fluids To Intervene
Osm
Fluid [Na] [K] [Cl] Buffer Ca Mg Tonicity (mOsm/ pH
L)
Plasma 135-145 3.5-5 95-105 23-30 2.5 1 290 7.35-7.45
LR 130 4 109 28 2.7 273 273 6.0-7.5
NS 154 0 154 0 0 0 308 308 4.5-7.0
NS 77 0 77 0 0 0 154 154
D5 NS 77 0 77 0 0 0 154 406 3.5-6.5
D5 NS 154 0 154 0 0 0 308 560 3.5-6.5
D5W 0 0 0 0 0 0 0 252 3.5-6.5
3% HTS 513 0 513 0 0 0 516
Plasma-
lyte 140 5 98 50 0 1.5 295
Sodium: If you correct >0.5mEq/hr
Pauls Case 2
A 90 y/o female with advanced dementia is brought to the ED by her
children with failure to thrive. She is non-verbal and had been
having difficulty swallowing clear liquids and solid foods for the past
few months. Family has been noting that she appears more
confused and having very dark urine.
In ED, 37.2, HR 110, BP 90/60, RR 14, O2 sats 93% on RA
ED said she was dehydrated and gave a bolus of 1L normal saline,

and admitted to Wearn.
Case 2 Continued
Physical exam shows a frail, elderly female who is responsive only
to painful stimuli and loud voice, but does open her eyes. A&Ox1.
Dry, cracked mucus membranes, severely decreased skin turgor,

incontinent of dark urine, stage 2 sacral decubitus ulcer
Case 2 Continued
Physical exam shows a frail, elderly female who is responsive only
to painful stimuli and loud voice, but does open her eyes. A&Ox1.
Dry, cracked mucus membranes, severely decreased skin turgor,

incontinent of dark urine, stage 2 sacral decubitus ulcer
RFP 161/4.6/129/22/45/2.2 (baseline 1.4) <80
Serum Osm 330, Urine Osm 400, Urine sodium 100

Basics on Hypernatremia
Less common than hyponatremia
Associated with high mortality (some studies suggest 40-60%)
Due to combined water & electrolyte deficit, but loss of free water
exceeds the loss of electrolytes
Most common in patients with decreased thirst and/or decreased

access to fluids
Hypernatremia:
Clinical signs and symptoms
Nausea/vomiting
Restless, irritable, or lethargic
Anorexia
Stupor/coma
Subarachnoid hemorrhage--Why?
Working Up Hypernatremia

History

History and Physical

Based on Urine Osm, Urine Electrolytes
Working Up Hypernatremia

History

Almost always hypovolemic

Is the urine concentrated?
If Yes likely 2/2 free water deficit from insensible, GI or renal losses
If No likely 2/2 diuretics or diabetes insipidus (either central or nephrogenic)

Sodium: Hypernatremia
Hypernatremia: Causes
Free water loss
Diuretics (loop)
Post obstructive diuresis
Acute and chronic renal disease
Sweating, fistula, burns, diarrhea, vomiting
Diabetes insipidus (central, nephrogenic)
Sodium gain
Hypertonic saline or sodium bicarbonate
TPN
Hyperaldosteronism
Cushings syndrome
Sodium control and effects
Some math:
TBW deficit:
Men: (140-(Na)/140 * TBW
Women: (140-(Na)/140 * TBW
Effect of IV fluids:
Change in Na per L of fluid= ([Na](solution) [Na](serum)) / (TBW+1)
Sort of like C1V1=C2V2
Hypernatremia: Therapy
Up front: Risk of seizures and cerebral edema if corrected
too rapidly
Correct hypovolemia with NS
Correct Na with 0.45% NS
Check Na frequently and adjust fluid therapy for a goal of

0.5-1mEq/L decrease every hour
Probably aiming for 48-72hr correction
Remember to think about ongoing losses

Urine replacement (w/ 0.45% NS or even 0.22% NS)
Vasopressin for central DI

Sodium: If you correct >0.5mEq/hr
Case 2 Continued
The patient was started on normal saline in the ED at 100 cc/hr and
admitted to the floor
Upon arrival to the floor, repeat RFP shows a sodium of 162.
You calculate a free water deficit of 3.9L
Change [Na]/L of fluid= ([Na](solution) [Na](serum)) / (TBW+1)

Lets call her current TBW ~19kg
Fluids To Intervene
Osm
Fluid [Na] [K] [Cl] Buffer Ca Mg Kcal/L (mOsm/ pH
L)
Plasma 135-145 3.5-5 95-105 23-30 2.5 1 290 7.35-7.45
LR 130 4 109 28 2.7 273 6.0-7.5
NS 154 0 154 0 0 0 0 308 4.5-7.0
NS 77 0 77 0 0 0 0 154
D5 NS 77 0 77 0 0 0 0 406 3.5-6.5
D5 NS 154 0 154 0 0 0 0 560 3.5-6.5
D5W 0 0 0 0 0 0 252 3.5-6.5
3% HTS 513 0 513 0 0 0 516
Plasma-
lyte 140 5 98 50 0 1.5 295
Case Conclusion
You start the patient on D5W infusion at 65 cc/hr

Monitoring RFPs Q8H.
Her deficit improves appropriately over 72 hrs as does her mental

status
Speech therapy finds that the patient has mild dysphagia and she is
discharged to SNF on a dysphagia diet.
Sodium
What to ponder Hypo Hyper
Most common situation Lab findings, nausea, HA Lab findings, irritability
Most dangerous situation Seizures, cerebral edema Hemorrhage, Coma
Most common cause Sweat, diuretics, meds, SIADH Sweat, diuretics, renal dz
CHF/Cirrhosis/Renal failure plus

Most dangerous cause Burns, Endocrine issues
an acute issue to decompensate
Best way to fix Fluids Fluids

Conclusions so far:
Sodium: Easy for the body; body in trouble = so is your brain
Process: Timeline, Volume Status, (Osmoles), and Bodys Response
NF called to Carpenter
Nurse is very concerned, patient feels off and is not herself.
Arriving bedside, pt is agitated and says her heart feels weird and
says why havent you all fixed this yet? She tries to wave at you
but seems to be moving very weakly.
The patient is a 58yo w/ severe DM-2 and AKI on CKD admitted for
osteomyelitis of her toe.
Pt took her Lisinopril right up to admission
Shes snacking on nuts, avocadoes, and lots of greens
Hyperkalemia: Symptoms
Symptoms
Muscle weakness/paresthesias
EKG changes:
Peaked T waves
Prolonged PR interval
Widened QRS
Sine wave
V-fib
Hyperkalemia: Causes
Trans-cellular shift
Acidosis (H for K), digitalis overdose, somatostatin
Impaired excretion
Renal failure, mineralocorticoid deficiency, drugs, type IV RTA,
Iatrogenic
Cell destruction
Crush injuries, Rhabdomyolysis, Tumor lysis
Hyperkalemia: Treatment
Intervention Dose Onset Comment
Calcium gluconate
1-2 amps IV <3 min Lasts 30-60 min
Calcium chloride*
Bicarbonate 1-3 amps IV 15-30 mins Lasts 30 mins
B2 agonists Alb 10-20mg inh.

Full in 30-90 mins Lasts 120 mins
(~4-8x neb dose) Or 0.5mg IV
10U IV with
Insulin/Glucose Full in 15-30 mins Lasts 60 mins
1-2 amps D50W
Kayexalate 30-90g PO/PR 1-2 hours Lasts 6 hours
Diuretics Lasix >40mg IV 30 mins Lasts 6 hours
Whenever access can

Hemodialysis AEIOU, right?
be attained
MICU rounds
36yo came w/ septic shock, (DIC, acute heart failure, cirrhosis); s/p
loads of fluids and ABX for treatmentanasarca has set in
Diuresing rapidly, has diarrhea, given B2-agonists frequently
K 2.6
How do you want to fix this?

Hypokalemia: Signs and symptoms
Generalized muscle weakness
Paralytic ileus
Cardiac arrhythmias
Atrial tachycardia
AV dissociation
EKG changes
Flat/inverted T waves
ST segment depression
U waves
Ascending paralysis and impaired respiratory function (K<2)

Potassium control and effects
Potassium control and effects
Hypokalemia: Causes
Transcellular shift
Alkalosis, beta agonists, caffeine, insulin, thyrotoxicosis
Renal loss
Primary hyperaldosteronism, hypothermia, genetic syndromes (i.e. Liddles),
type I and II RTA, drugs (i.e. amphotericin, foscarnet)
GI loss
Vomiting, diarrhea
(and VIPoma, enteric fistula, malabsorption, jejunoileal bypass)
Fluids To Lose (from Maxwells)
Volume
Fluid [Na] [K] [Cl] [HCO3]
(mL/day)
Salivary 10 26 10 30 500-2000
Gastric 60 10 140 0 100-4000
Biliary 145 5 100 35 50-800
Pancreatic 140 5 75 115 100-800
Ileal 130 5 100 50 100-9000
Diarrheal 60 35 40 30 Varies
Hypokalemia: Treatment
Supplement:
KCl: Each 10 mEq raises K by 0.1mEq/L (if 3.0 or above)
Usually give 40mEq at one time, re-measure later
PO route: Causes gastric upset
IV route: Caustic to veins, hurts even run slowly (if PIV)
Hemodialysis: high K bath can restore
K Phos, K Citrate are available, gentler

40% as efficient as KCl
Is what is found in fruits
Bananas: 1cm~1mEq of K
For 40 mEq, need 2-3 bananas
University Hospitals of Cleveland Adult Electrolyte

Replacement Guidelines (Rev 6/17/2004)
Potassium
Most common situation Weakness, ileus Irritability
Most dangerous situation Arrhythmia, death VT, death
Most common cause Diarrhea, diuretics, insulin Renal failure
Most dangerous cause Alkalosis, severe fluid losses Tumor lysis, Rhabdo
PO=IV, pick your poison based on

Best way to fix Shift, then think total stores
the speed and person
Conclusions so far
Potassium: Heart wants you to know that its all about balance
ICF-ECF balance is crucial; Shifts vs Depletion/Overload; PO upset, IV burns
Another Case
Patient recovering from severe gastroenteritis w/ vomiting, diarrhea
Eating and drinking still diminished despite tons of Zofran IV
IV fluids, ~80mEq KCl per day for diarrheal losses.
They complain of hand tremors and tingling today
RFP: 145/3.2/110/20/20/0.8, Ca 8.3, Phos 2.6, Alb 3.5

Another Case
Patient recovering from severe gastroenteritis w/ vomiting, diarrhea
Eating and drinking still diminished despite tons of Zofran IV
IV fluids, ~80mEq KCl per day for diarrheal losses.
They complain of hand tremors and tingling today
RFP: 145/3.2/110/20/20/0.8, Ca 8.3, Phos 2.6, Alb 3.5

Magnesium level is added on, found to be 0.8
Magnesium control and effects
Location:
~55% in bone, ~44% in cells,
~1% in ECF;
~2/3 ionized, ~1/3 protein-bound;
tiny amount complexed
Normal [Mg] 1.52.4 mg/dl
Magnesium: Hypomagnesemia
Causes
Malnutrition / alcoholism
GI losses (diarrhea, vomiting)
Renal losses (e.g. diuretics, cisplatin, cyclosporine, proton pump inhibitors)
Hyperaldosteronism
At particular risk are alcoholics and critical care patients
Symptoms:
Less than 1.5 mg/dl: Confusion, NM excitability,
HypoK, HypoCa: Mg prevents kidneys from getting rid of these
Severe when Mg < 1.0 mg/dl
Tremor, tetany, convulsions, weakness, delirium, coma.
Can cause torsades de pointes, arrhythmias, seizures, death
Treatment
PO or IV magnesium:
PO causes diarrhea
IV is far better, especially if slow
Calcium gluconate for tetany
Only ~1/6
absorbed /
bioavailable
Go even
slower!


Magnesium: Hypermagnesemia
Causes
Renal failure
Increased Mg intakeincludes MgSO4 (for HypoMg or PIH/eclampsia)
Acute adrenocortical insufficiency
Hypothermia
Clinical manifestations:
Mg 4-6: N/V, flushing, headache, lethargy, drowsiness; Diminished DTRs
Mg 6-10: Somnolent, HoTN, bradycardia, ECG changes, HypoCa; Absent DTRs
Mg>12: Paralysis/flaccid quadriplegia; Apnea, respiratory failure
Complete heart block. Cardiac arrest
Treatment
IV calcium (chloride or gluconate) to oppose magnesiums dangerous effects
Stopping intake
Increasing fluids with diuretics or dialysis if renal failure
Magnesium
Most common situation Confusion, HypoK, HypoCa Flushing, headache
Most dangerous situation Tremor, Sz, Torsades, Death Respiratory failure, heart block
Most common cause Renal and GI losses Renal failure, or Iatrogenic
Most dangerous cause Alcoholism w/ Renal, GI losses Renal failure, adrenal insuff
Best way to fix Replete, IV if possible, PO gently IV Ca, low intake, high urine
Conclusions so far
Magnesium: Potassiums cousin. Acts like it, moves with it.

Measure when having K troubles; PO=diarrhea, Slow IV drip is best
Chloride: control and effects
Main ECF anion
High levels in CSF, bile, pancreatic
fluid
Helps maintain ECF osmolality

Directly related to Na
Helps maintain acid-base

balance;
Inversely related to HCO3-
Chloride
Most common situation Agitation, labs off Weakness, labs off
Most dangerous situation Coma, Arrhythmia LOC, Coma
Most common cause Hypotonic fluids, dehydration Hypertonic fluids, meds
Metabolic alkalosis
Most dangerous cause Metabolic Acidosis
(hypochloremic versions)
Best way to fix Salty intake, Tx underlying Dx Limit salt, consider diuretics
Conclusions so far

Chloride: Sodiums shadow, tells you secrets about HCO3

America loves salt. IV fluids: Not thinking about solution=part of the problem
NF to Dworken
Called to room for feeling numb
70yo w/ CKD-2, DM-2, CHF, EtOH abuse: presents w/ GI bleed

Anemic and fluid overloaded, s/p 4U pRBC and Lasix 80mg IV BID
At bedside, patient having cannot feel his lips, feels like his
fingers/legs are numb, but also seems to be having tremors.
Patient is extremely irritable.

NF to Dworken

RFP: 132/3.6/88/36/36/1.25, Ca 6.6, Phos 3.2, Alb 2.0
NF to Dworken

RFP: 132/3.6/88/36/36/1.25, Ca 6.6, Phos 3.2, Alb 2.0

Ca Correction = [Ca] + (0.8*(4.0-Alb)); so 6.6 + 0.8*(2.0) makes 8.2
Calcium control and effects
Location:
Teeth and bones (99%, w/ Phos)
Found in cell membranes
[ICF] ~ [ECF]
Ionized (active)
Protein bound
Function:
Affects cell membrane permeability
and firing level
Muscles need calcium to contract
Helps coagulation
Hypocalcemia
Symptoms appear when iCa <0.7
Symptoms include:
Circumoral numbness; Paresthesias; NM irritability (tetany), Diarrhea,
Anxiety/Confusion; Hypotension, Laryngospasm/bronchospasm; Rickets
EKG changes include:

Prolonged QT
Non-specific ST-T wave changes
Calcium: Hypocalcemia
Causes:
Total body calcium decrease:
Decreased albumin: Ca Correction = [Ca] + (0.8*(4.0-Alb))
Chronic renal failure or alcoholism
Renal/GI losses (pancreatitis, diarrhea)
Deficiencies in Magnesium or vitamin D; Elevated phosphorus
Hypo PTH
Ionized calcium decrease:
Alkalosis, large amounts citrated blood or Hemodilution
Calcium chelation/precipitation
Tumor lysis, rhabdomyolysis, citrate, foscarnet
Multifactorial
Sepsis, pancreatitis, burns
Hypocalcemia: Causes and Diagnosis
Determine the cause
PTH level
Vitamin D levels (25OHD3 and 1,25OHD3)
24 hour urine calcium
Hypoparathyroidism
Irradiation, surgery, hypomagnesemia, DiGeorge, polyglandular autoimmune
syndrome, storage disease, HIV
Vitamin D deficiency
Malnutrition, malabsorption, hepatobiliary disease, low sun exposure
Hypocalcemia: Treatment
Treat low Magnesium, high Phos if co-existing
Treat underlying disease
Calcium gluconate
25-100mg/kg IV
Calcium chloride
10-20 mg/kg IV
Must be given centrally; otherwise, burns severely (used in codes)
If replacing, IV calcium and PO Vitamin D

When should you avoid treating hypocalcemia?
Tumor lysis syndrome (unless patient is symptomatic)
Another case
80yo patient w/ cough, R shoulder pain, presents to ED
Patient appears dehydrated, reports polyuria and constipation

Another case
80yo patient w/ cough, R shoulder pain, presents to ED
Patient appears dehydrated, reports polyuria and constipation
RFP: 138/3.8/102/24/10/0.4, Ca 9.6, Phos 2.2, Alb 2.0

Calcium: Hypercalcemia
Causes:
Total calcium elevated:
High intake or intestinal absorption (e.g., vitamin A & D overdose)
Bone release (hyper-PTH, malignancies, prolonged immobilization)
Decreased excretion (diuretics)
Ionized calcium (iCa++) elevated
Acidosis
Decreased neuromuscular action, GI motility;
Increased cardiac irritability (short QT & ST, ventricular arrhythmias)
Renal stones, polyuria
Treatment:
Decrease intake, rapid hydration (PO or IV), IV phosphate to bind
Loop diuretics; Drugs to decrease bone resorption (e.g., calcitonin, EDTA)
Dialysis if renal failure
Calcium
Most common situation Circumoral numbness Weakness, constip, stones
Most dangerous situation Prolonged QT Ventricular arrhythmias
Most common cause Diuresis, CKD, Vit D def Bone release
Most dangerous cause Tumor lysis, rhabdomyolysis Bone releasemalig
Best way to fix Supplements, Tx underlying Dx Hydration, Phos, Diuresis, HD
Make sure you fix Mg, Vit D

Conclusions so far


Calcium: Musculoskeletal master, whole body deal, loves proteins

Low? Replete. High? Dilute, distract, dump. But you need to find a diagnosis
Last case/wrap up
70yo ESRD patient w/ NHL just started treatment outpatient
treatment, was found down at home on morning of HD, was brought
to ED instead.
Patient dehydrated, tachycardic, extremely anxious, cramping,

EKGs shows rhythms that scare you
Last case/wrap up
70yo ESRD patient w/ NHL just started treatment outpatient
treatment, was found down at home on morning of HD, was brought
to ED instead.
Patient dehydrated, tachycardic, extremely anxious, cramping,

EKGs shows rhythms that scare you
RFP: 133/5.6/100/18/55/6.0/98, Ca 5.2, Phos 9.6, Alb 3.6

Phosphate control and effects
Location: ~85% in bones &
teeth, 14% soft tissue; <1%
ECF
Function:
Major ICF anion
Energy storagethink ATP
Metabolism of carbohydrates,
proteins, and fats
H+ buffer
Oxygen transport
WBC and platelet function
Phosphate: Hyperphosphatemia
Causes:
Shifts:
Respiratory acidosis, untreated DKA
Actual overload
Mostly renal insufficiency/failure, decreased urinary losses (hypoPTH, hypovolemia)
Increased intake
Cell destruction (chemotherapeutic agents, increased catabolism, rhabdomyolysis)
Majority related to hypocalcemia
Early: Oliguria, corneal haziness, conjunctivitis, irregular HR, dysrhythmias,
conduction problems, papular eruptions
Late: Metastatic calcifications of CaPhos into soft tissues, joints, & arteries
Treatment:
Decreasing phosphorus intake & absorption, giving fluids, dialysis if needed
I lied. Last case
22yo w/ Hx of anorexia and alcoholism, hospitalized and under
observation, now complaining of shortness of breath
IVF initially; diet of numerous Boost shakes, scant food
Vitals initially showed bradycardia and low BMI;

Today HR 78, looks puffy today, shaky/weak,
RFP: What do you expect?

I lied. Last case
22yo w/ Hx of anorexia and alcoholism, hospitalized and under
observation, now complaining of shortness of breath
IVF initially; diet of numerous Boost shakes, scant food
Vitals initially showed bradycardia and low BMI;

Today HR 78, looks puffy today, shaky/weak,
RFP: 142/2.7/102/26/6/0.3/78 Ca 8.0, Phos 1.2, Alb 1.5

Phosphate: Hypophosphatemia
Causes: Dangers from refeeding, alcoholism, DKA s/p Tx, burns
Transient shift into cells, usually with tissue repair:
Refeeding syndrome, Resp Alkalosis, Catecholamine surges, Burns, Hypothermia,
androgen
Losses
Renal losses (Diuretics, hypomagnesemia, hypokalemia, hyperparathyroidism);
Decreased intake/intestinal absorption, or increased intestinal loss
Clinical manifestations
Most secondary to decreased ATP & 2,3-DPG
Muscle weakness, paralysis
Respiratory depression
Hemolysis, Leukocyte and platelet dysfunction
Treatment: PO and IV phosphorus products

Phosphate
Most common situation Muscle weakness Oliguria, Hypocalcemia
Most dangerous situation Respiratory depression Irregular HR, Calcifications
Most common cause Alcoholism, burns Renal failure
Most dangerous cause Refeeding syndrome Rhabdomyolysis, tumor lysis
Best way to fix High intake, repletion Low intake, High fluids, HD
Conclusions so far


Calcium: Musculoskeletal master, whole body deal, loves proteins

Low? Replete. High? Dilute, distract, dump. But you need to find a diagnosis
Phosphate: Frenemy of calcium but lets you breathe, move.

Comes with an RFP; make sure it stays normal; use the diet
Fluids To Intervene
Osm
Fluid [Na] [K] [Cl] Buffer Ca Mg Kcal/L (mOsm/ pH
L)
Plasma 135-145 3.5-5 95-105 23-30 2.5 1 290 7.35-7.45
LR 130 4 109 28 2.7 273 6.0-7.5
NS 154 0 154 0 0 0 0 308 4.5-7.0
NS 77 0 77 0 0 0 0 154
D5 NS 77 0 77 0 0 0 0 406 3.5-6.5
D5 NS 154 0 154 0 0 0 0 560 3.5-6.5
D5W 0 0 0 0 0 0 252 3.5-6.5
3% HTS 513 0 513 0 0 0 516
Plasma-
lyte 140 5 98 50 0 1.5 295
So why not LR?
Crystalloids: Buffered vs Normal Saline Family

we cant possibly cover this whole battle
Cochrane review 2012: LR vs NS in peri-operative patients

No difference in mortality, renal function, blood blood
Paper comparing LR and NS found benefit in pancreatitis

The importance of Beta comes in herenot a big study, dont extrapolate
15% arterial (1-2% of all TBW)
This is where we need fluids to help perfusion/shock
85% is venous (5-7% of all TBW)
This is where we get most of our measurements
This is where we infuse fluids
How far do we want the fluids to go?
If fluids get through heart and lungs without any changes,

we have expanded arterial circulation
So how do we get fluids to stay?
Isotonic crystalloids
28 healthy volunteers, given 10-30mL/kg of NS
After 30 mins, 64% of infused volume had already left IV compartment
Pre-surgical and healthy volunteers, got 2L NS over 1-2h
Immediately after infusion done, Intravascular retention of 18-24% (by Hct)
6hr after infusion, 60% of fluid volume in body; IV retention of 13%
Colloids:
Stays in IV compartment longer
If using NS, will need 40% more volume
(Finfer S, Bellomo R, Boyce N et al. A comparison of albumin and saline for fluid
resuscitation in the intensive care unit. N Engl J Med 2004; 350: 22472256)
Colloids vs Crystalloids
we cant possibly cover all this
Cochrane review 1998: Albumin vs Crystalloids
Albumin conferred higher risk of death, RR of 1.68 (p<0.01)
SAFE trial (Saline versus Albumin Fluid Evaluation)
~7000 ICU-admitted adults, 4% albumin vs NS
No mortality difference between NS, Albumin overall
Subgroup of Traumatic Brain Injury? Albumin had higher mortality
Subgroup of Severe Sepsis: Albumin had lower mortality
CRISTAL study, 2857 patients getting all colloid or all crystalloid

No difference in 28-day mortality
90-day mortality lower in colloids (P=0.03 but RR 0.92, 95% CI 0.86-0.99)
Cochrane in 2011 redid the Albumin vs NS study, included SAFE
No mortality difference!
Fluid Needs
Maintenance
Normal daily outputs
Urine = 12-15 cc/kg
Stool = 3 cc/kg
Sweat = 1.5 cc/kg
Respiratory and Skin insensible
losses = 10 cc/kg
Increased by 8%/degree F for fever
Normal daily endogenous input
Oxidation of carbohydrates and fat =
3 cc/kg
References used (beyond notes in slides)
Severs E, Hoorn EJ, Rookmaaker MB. Nephrol Dial Transplant (2015) 30: 187
196 doi: 10.1093/ndt/gfu104
Braun et al. Diagnosis and Management of Sodium Disorders: Hyponatremia and
Hypernatremia. Am Fam Physician 2015 Mar 1;91(5):299-307.
Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in
critically ill patients. Cochrane Database Syst Rev 2013; 2: CD000567
Sterns RH. Disorders of Plasma Sodium Causes, Consequences, and
Correction. N Engl J Med 2015;372:55-65. DOI:10.1056/NEJMra1404489
Gumz ML, Rabinowitz L, Wingo CS. An Integrated View of Potassium
Homeostasis. N Engl J Med 2015;373:60-72. DOI: 10.1056/NEJMra1313341
Mortiz ML, Ayus JC. Maintenance Intravenous Fluids in Acutely Ill Patients. N
Engl J Med 2015;373:1350-60. DOI: 10.1056/NEJMra1412877
University Hospitals of Cleveland Adult Electrolyte Replacement Guidelines (Rev
6/17/2004)

Fluids and Electrolytes Keith Torrey

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Electrolytes (and fluids)

Electrolyte disturbances: very common, can be dangerous!

BMP Na/K/Cl/HCO3/BUN/Cr/Glu/Ca $206 Nope

RFP All of BMP + Phos, Alb $96 Yes

Na $78 K $78 Cl $51 Phos $32 Mg $90 Ca (ionized) $140

For good measure:

Moderate to severe HAA developed in 3551 patients (20%).

For every 50 mL of blood drawn, the risk of moderate to severe HAA

Each 1mL of blood drawn decreases hemoglobin by ~0.07 g/dL

(Paul Shaniuk is the greatest for contributing this slide)

Because this tiny corner

25% of this is IVF/Plasma (Its ~1/12 of TBW, ~5-8%)

Where the electrolytes are found (Helps w/ Dx and Tx)

Hypo: Problems, recognition, diagnosis, correction

Hyper: Problems, recognition, diagnosis, correction

No significant family, medical or social history except for alcoholism. Only

(Paul Shaniuk is the greatest for contributing this case)

No significant family, medical or social history except for alcoholism.

BMP 125/4.1/87/28/6/0.64<102. Negative CXR & UA.

2. Volume status: Hypovolemic, Euvolemic, Hypervolemic?

Neurologic exam showed b/l nystagmus with lateral gaze and

2. Volume status: Hypovolemic, Euvolemic, Hypervolemic?

3. Think about Serum Osm and its components

4. Is the body responding appropriately or inappropriately?

Urine osmolarity 600

Urine sodium - 166

2. Volume status: Hypovolemic, Euvolemic, Hypervolemic?

3. Think about Serum Osm and its components

4. Is the body responding appropriately or inappropriately?

Picture was clouded by the fact that he was presumed to have

Acute change: Can correct quickly

Chronic change: Need to correct slowly

Check frequent sodiums (q1 or q2h)

Can correct rapidly w/ 3% NS in severe symptomatic

Normalize sodium at a rate of 8-12 mEq/L per 24h

Rise in [Na]/L = ([Na](solution) [Na](serum)) / (TBW+1)

Check frequent sodiums (q1 or q2h)

In ED, 37.2, HR 110, BP 90/60, RR 14, O2 sats 93% on RA

ED said she was dehydrated and gave a bolus of 1L normal saline,

Dry, cracked mucus membranes, severely decreased skin turgor,

Dry, cracked mucus membranes, severely decreased skin turgor,

RFP 161/4.6/129/22/45/2.2 (baseline 1.4) <80

Serum Osm 330, Urine Osm 400, Urine sodium 100

Associated with high mortality (some studies suggest 40-60%)

Most common in patients with decreased thirst and/or decreased

1. Think about risks, time courseover weeks or over hours?

2. Volume status: Hypovolemic, Euvolemic, Hypervolemic?

3. Is the body responding appropriately or inappropriately?

1. Think about risks, time courseover weeks or over hours?

2. Volume status: Hypovolemic, Euvolemic, Hypervolemic?

3. Is the body responding appropriately or inappropriately?

If No likely 2/2 diuretics or diabetes insipidus (either central or nephrogenic)

Check Na frequently and adjust fluid therapy for a goal of

Remember to think about ongoing losses

Vasopressin for central DI

Upon arrival to the floor, repeat RFP shows a sodium of 162.

You calculate a free water deficit of 3.9L

Change [Na]/L of fluid= ([Na](solution) [Na](serum)) / (TBW+1)

You start the patient on D5W infusion at 65 cc/hr

Her deficit improves appropriately over 72 hrs as does her mental

Most common situation Lab findings, nausea, HA Lab findings, irritability

Most dangerous situation Seizures, cerebral edema Hemorrhage, Coma

CHF/Cirrhosis/Renal failure plus

Best way to fix Fluids Fluids