Fluid & Electrolyte Disorders

Potassium
Also contains phosphate, magnesium, and proteins

Sodium

The liquid portion of blood within blood vessels

The fluid in the microscoptic space between cells

tachycardia
hypotension
oliguria (low urine output)
AMS (altered mental status)
dry mucus membranes

Edema

More total body water than total body solutes… watery, low sodium concentration

More total body solutes than total body water… salty, high sodium concentration

Decreased osmolality of the ECF

Ideal osmolality of the body (~290 mOsmol/L)

Increased osmolality of the ECF

Non enough TBW (total body water), low volume

Ideal TBW

To much TBW, high volume

No symptoms
Headache
Nausea
Vomiting
Fatigue
Confusion
Muscle cramps

Headache
Nausea
Vomiting
Fatigue
Confusion
Muscle cramps

Lethargy
Seizures
Brain herniation
Death

Patients with hyponatremia will be hypotonic, since they don't have enough solutes in their ECF.

However, they may be hypertonic if they also have hyperglycemia.
They may also be isotonic if they have hypertriglyceridemia.

Diarrhea
Diuresis
Excess sweating

(Water leaves the body along with solutes, leading to hypotonicity and hypovolemia)

CHF (chronic heart failure) which can cause fluid overload, hypervolemic. low cardiac output leads to poor renal perfusion, which activates arginine vasopressin. This leads to free water absorption, increasing hyponatremia

Cirrhosis, kidney impairment leads to disproportionate water retention as compared to sodium, too much sodium is eliminated while water stays in the body, also activates arginine vasopressin, which increases free water absorption and hyponatremia

AKI (Acute kidney injury)/CKD (Chronic kidney disease)/HD (hemodialysis), fluid overload due to difficulty excreting urine (hypervolemia), fluids used in hemodialysis (dialysates) are hypotonic

SAIDH (Syndrome of inappropriate antidiuretic hormone secretion), the body makes too much ADH, which can lead to some fluid retention while keeping sodium excretion.

Antidepressants (SSRIs and SNRIs are common culprits)

Anticonvulsants

Antipsychotic agents

isotonic saline (normal saline), water will be retained while the sodium is excreted, worsening hyponatremia

Goal of increasing sodium concentrations by 4 to 6 mEq/L every 24 hours, with a max of 8 mEq/L increase every 24 hours, to avoid osmotic demyelination syndrome (ODS), which can occur if sodium concentrations occur too rapidly.

Address underlying causes
Discontinue hypotonic fluids
Discontinue medications causing hyponatremia
If life threatening, administer hypertonic saline (NaCl 3%)

Thiazide diuretics
Excessive use of hypotonic fluids (continuous fluids, IV bactrim, IV Heparin)
Many psychiatric medications can cause SAIDH

Central line, peripheral line infiltration can lead to tissue necrosis

To correct hyponatremia only in life threatening situations. High risk treatment option.

Isotonic crystalloid solutions (Noramal saline or lactated ringers) to replenish TBW without affecting sodium concentrations

Fluid restriction of less than 800mL/day
Slightly increased sodium intake and drink sports beverages
Loop diuretics to decrease TBW (bumetanide, furosemide, and torsemide)

Some risk of increasing hyponatremia (balanced by increased sodium intake), however much lower risk compared to thiazide diuretics, and they effectively reduce TBW

Sodium chloride tablets (dose can be determined by the sodium deficit calculation)
Urea (induces free water excretion, normalizing sodium levels)
Vasopressin antagonists (tolvaptan and conivaptan) (promotes excretion of free water, however onset of action is too slow to be used in an acute setting and there is variable efficacy, not commonly used)

The serum sodium concentration that would result from a patient with hyperglycemia's glucose level was reduced to a normal range.

Decreased fluid intake

Sodium overload
Mineralocorticoid (aldosterone) excess

Diabetes insipidus

Address underlying cause
Administer hypotonic fluids (D5W, 1/2NS, D51/2NS)
Add diuretics (loop or thiazide, no longer worried about causing hyponatremia) for hypervolemic patients)
Watch electrolytes, dextrose and diuretics can cause potassium shifts

Lack of or lack of response to antidiuretic hormone (ADH), which causes constant urination and thirst.

Damage to hypothalamus or pituitary gland causing a lack of production or storage of ADH

Arginine vasopressin deficiency (AVP-D)

Kidneys don't properly respond to ADH, often caused by lithium

arginine vasopressin resistance (AVP-R)

Desmopressin (DDAVP), a synthetic analogue of ADH, causing water reabsorption and a lowering of sodium concentration

0.25 to 1mg SC/IV every 12 to 24 hours (also available IN, PO, and SL)

Insulin (causes cellular absorption of potassium, lowering concentration in ECF)
Inadequate intake, malnourishment
Vomiting, diarrhea, laxatives
Hypomagnesemia (promotes potassium loss in kidneys)
Loop diuretics

Renal failure
K sparing diuretics
ACE, ARB, NSAIDs
Trauma

Address underlying causes
Increase dietary consumption (bananas, beets, potatoes)
Oral potassium supplementation
IV K supplementation

A glass of water to reduce stomach upset

KCl 20mEq/15mL oral liquid
Klor-Con powder, 20mEq packet
Klor-Con K tab, large wax matrix ER tablet
Klor-Con M tab, microencapsulation that may be dissolved in water
8, 10, 15, and 20mEq doses available

Kphos is also available if phosphorous is low in addition to potassium

0.1 mg/dL K serum increase per 10mEq PO or IV, greater increase in renal dysfunction

10-40 mEq/day chronic outpatient

20-40 mEq one time inpatient, then more given every few hours as needed. Usually limited to 60mEq/dose to avoid GI upset

IV KCl available in 10, 20, or 40 mEq bags

10mEq/50mL administered via peripheral line @ 10 mEq/hr
20mEq/50mL administered via central line @ 20 mEq/hr
Doses higher than 20mEq/hr require continuous EKG monitoring
if phlebitis (inflammation of a vein) or infusion pain occur, give slower or more diluted
Can also be given in some maintinence IV fluid mixes

when there are Clinical manifestations or ECG changes

K > 6.5 meq/L

K > 5.5 meq/L plus kidney function impairment or ongoing tissue breakdown or K absorption

If it is an emergency, give IV calcium gluconate or IV calcium chloride IV push ASAP. This stabilized cardiac cells by decreasing membrane depolarization. Can cause arrythmias so give in emergency only

If it is not an emergency, consider administering calcium gluconate over 15 – 60 minutes, but check calcium first

these effects only last 30-60 minutes, so continue with additional treatment below

Insulin + dextrose IV, this causes increased activity of the Na-K-ATPase pump in skeletal muscles, bringing more K into cells and out of the ECM. Dextrose is given to mitigate hypoglycemia and is not needed in hyperglycemic patients

Hemodialysis in patients with ESRD

Gastrointestinal cation exchanger (K binder) which removes K via fecal excretion, can be used for chronic hyperkalemia

Address underlying cause

1g IV calcium gluconate or 1g IV calcium chloride IV push ASAP for emergency hyperkalemia.

If not an emergency, can consider administering over 15-60 minutes, but check calcium first.

10 units IV regular insulin immediately followed by 50 mL of 50% dextrose (25g glucose)

5 units

10 units insulin lowers K by ~1 mEq/L in 15 minutes, lasting 4-6 hours

Glucose should be measured every 4 – 6 hours to monitor for hypoglycemia (occurs in 20% of patients)

Sodium zirconium cyclosilicate (Lokelma)

Patiromer (Veltassa)

Kayexelate (Sodium polystyrene sulfonate) is not used often anymore due to high rates of bowel obstruction and perforation

Renal dysfunction

Magnesium supplements

Alcohol use disorder

GI losses

Renal losses

Drugs

Amphotericin B
diuretics
PPIs

Address the underlying cause

Cessation of magnesium-containing products (supplements, antacids, laxatives, over-replacement)

Loop diuretics

If concerns of cardiac abnormalities, administer IV calcium gluconate

Hemodialysis

Address the underlying cause

Oral magnesium, or IV if not tolerated

Magnesium oxide 400 mg by mouth once daily

Or 2g IV over 1 hr if not tolerated

Reduce dose by 50% in renal dysfunction

Calcium is highly protein bound, so in practice we correct for albumin

Corrected Ca mg/dL = (0.8 * (4 - Pt's Albumin)) + Serum Ca

Alcohol misuse
diarrhea
PTH abnormality
low active vitamin D
drugs

Phenobarbital
phenytoin
H2RAs
PPIs
steroids

Primary hyperparathyroidism
malignancy
drugs

Excessive antacid use

Excessive calcium supplementation

Lithium

Thiazide diuretics

Address the underlying cause
IV fluids, reduces concentration of calcium and helps with dehydration

Address the underlying cause
Administer IV calcium gluconate or IV calcium chloride, oral calcium used in asymptomatic or maintenence patients

1g IV calcium gluconate over 60 minutes preferred, do not IV push unless emergency

1g calcium gluconate will increase serum calcium by ~ 0.5

Reduced dietary phosphate intake

Diuretics

Alcohol use disorder

Phosphate-binding drugs

CKD-MBD (chronic kidney disease mineral bone disease)
Over-supplementation
Rhabdomyolysis
TLS (tumor lysis syndrome)

Address the underlying cause

IV phosphorous standard preparations given over 2 – 3 hours

Preparations will differ by institution

PO phosphorous used for asymptomatic or mild/moderate patients