FLUIDS AND ELECTROLYTES

Madison Feldman PGY-1

Wednesday, July 20, 2022
Preceptor: Dr. Kannan
TWIS Presentation
 OUTLINE

I. Fluid and electrolyte homeostasis

II. Hypokalemia and hyperkalemia
III. Hypocalcemia and hypercalcemia
IV. Hyponatremia and hypernatremia
V. Hypomagnesemia and hypermagnesemia
VI. Hypophosphatemia and hyperphosphatemia
 BODY FLUID
COMPARTMENTS

• Total body water (TBW)

60% of total weight
• 40% intracellular volume
(ICV) and 20% is
extracellular volume (ECV)
• ECV: interstitial fluid and
intravascular or plasma
volume (25% of ECV or 5%
body weight)
 MAINTENANCE BODY FLUIDS

• Sufficient water is required to replace obligatory urinary losses of 1000mL/day and GI losses of 100-200mL/day along with
insensible water losses
• Increased loss with hyperthermia and un-humidified air
• Daily intake:
• Sodium- 100-250mEq/day with loss through sweat, stool, and urine
• Potassium- 40-120mEq/day (0.5-0.8 mEq/kg/day) with 10-15% loss through urine
• Dextrose- 100mL of D5/hr avoids catabolism
• ~120g/day or 5g/hr to avoid catabolism
• D5 is 5% dextrose (5g/100mL) 4-2-1 Rule for Maintenance Fluids
• Maintain urine output Weight Rate Total rate
• Adults: 0.3-0.5 cc/kg/hr Four 0-10 4 mL/kg/hr 0 + 4 mL/kg/hr
kg
• Pediatrics: 1.0 cc/kg/hr
Two 10- 2 mL/kg/hr 40 + 2 mL/kg/hr
20kg
One >20 kg 1 mL/kg/hr 60mL/hr + 1 mL/kg/hr
 RESUSCITATIVE FLUIDS – ISOTONIC

• Normal Saline:
• slightly hypertonic, hypernatremic, and hyperchloremic
• used for volume contraction
• safe in renal failure or hyperkalemia
• Can cause hyperchloremic metabolic acidosis, hypotension, AKI
• Lactated Ringer:
• slightly hyponatremic/hypotonic
• electrolyte composition closer to physiologic
• used for resuscitation with metabolic acidosis
• cannot give with pRBCs due to calcium content
• Normosol (Plasmalyte) *LR and PL are balanced crystalloids because
they have Na, K, Cl closer to that of ECF and
• Balanced crystalloid
fewer adverse effects on pH (acid-base)
• Contains magnesium balance
• Caution in renal failure with high K and Mag and hypotension
EFFECTS OF CRYSTALLOID COMPOSITION
ON PLASMA ELECTROLYTES
 NORMAL SALINE VERSUS LR/PLASMALYTE

• Decrease in major kidney events for

balanced fluids
• Death, renal- replacement therapy and
persistent renal dysfunction
• SALT-ED Trial: 5.6% saline vs 4.7%
balanced crystalloid (CI 0.7-0.95, P=0.01)
• SMART Trial: 15.4% vs 14.3% (CI 0.82-
0.99, P=0.04)
• No difference between re-admission
rates
• Trend towards significance for
decreased mortality and decreased
incidence of new dialysis requirement
for ICU patients
 PLASMALYTE FINDINGS

• Drug interactions due to alkalinizing effects

• Renal excretion of acidic drugs increases and decreases in alkaline drugs
• False positives for pulmonary aspergillosis
• Not studied in pregnant, breastfeeding, or geriatric patients
• “Balanced fluid” and isotonic with plasma
• Decreased AKI after major abdominal surgery hypothesized from
hyperchloremia in NS patients
• NS causes reduced renal blood flow and reduced eGFR when compared to PL
• Use PL cautiously in hyperkalemia or hypo/hypermagnesia
• General surgery setting: not enough large-scale prospective trials
• Liver resection/transplant: PL vs Hartmann’s lower lactate, bilirubin,
PT, and high albumin

Plasmalyte: Na 140, K5, Mag 3, Cl 98, Acetate 27, Gluconate 23

 COLLOID

• Albumin, starches, whole blood, pRBC, and FFP

• Albumin: pancreatitis, burns, plasma loss from trauma
• Expensive and clinical evidence for benefit is weak
• No overall benefit and potentially increased mortality
 POTASSIUM

• Normal potassium: 3.5-5 mEq/L

• Replace when K <3.5, <4.0 in GI pts, <4.5 in cardiac pts.
• Make sure pt not in renal failure, replace magnesium additionally
• Prevention: identify sensible fluid losses and their electrolyte composition
• Sensible (diarrhea, NGT, or urine output)
• Insensible (water lost from skin, respiratory or open abdomen during lapartomy) (40-600mL in adult /
day)
• In diagnosis, look for acid-base abnormalities and free water changes
• Acidosis: increased K due to H+ ions being exchanged intracellular for K+
• Alkalosis: decreased K due to H+ ions being exchanged extracellular for K+
• Renal tubular acidosis – associated with K and H2O abnormalities
• Order: ECG, serum and urine testing
 HYPOKALEMIA

Risk Factors: Treatment:

• CHF, diuretics, diarrhea, vomiting, • 10 mEq per 0.1 increase in serum level desired
• PO preferred
enteric or pancreatic fistula losses
• Liquid – offensive taste
Symptoms: • Tablet – big pills
• Diminished or absent deep tendon • Dose typically 40mEq
reflexes, weakness • IV if unable to give via enteral access
• 10mEq/h through PIV
• Paresthesia, Paralysis
• 20mEq/hr through central line in monitored bed
• Skeletal muscle weakness • Consider concurrent hypomagnesemia or
• Constipation, Ileus hypocalcemia causing hypokalemia. Treating these
abnormalities will correct hypokalemia
• Abdominal pain 
• Cardiac arrhythmias
 HYPERKALEMIA

Treatment: C BIG K DROP

• Risk Factors:
C- Calcium Calcium gluconate (10%) 10 mL IV over 10 min
• Rhabdomyolysis
• Acidosis B- bicarbonate and Beta agonists: Salbutamol 10 - 20 mg in 4 mL normal saline nebulized over
beta agonists 10 min
• Muscle relaxants for anesthesia OR
Bicarbonate: Na bicarbonate 8.4% (50 mEq) 1 amp IV over 5 minutes
• Hyperpyrexia
I- Insulin Short acting insulin in 10 units pushed IV
• Hypoaldosteronism
• Symptoms: G- glucose D50W IV ampoule IV over 5 minutes given with insulin

• Muscle cramps, weakness, cramps

K-kayexalate Na polystyrene sulfonate 15-30g in 15-30mL PO
• Abd pain, Urine changes, diarrhea
• Respiratory distress D- diuretics Furosemide 40-80mg IV push

• EKG changes ROP- renal status of Dialysis

patient
• Decreased cardiac contractility
 POTASSIUM STATUS ON ECG

Hypokalemia: Hyperkalemia:
• Low-voltage, • Peaked T waves (typically
flattened, or at serum potassium >6
inverted T waves mEq/L)
• Prominent U waves • Flattened P waves
• Depressed ST • Increased PR intervals
segments • Decreased QT intervals
• Prolonged PR • Widened QRS complexes
intervals (at levels • Depressed ST segments 
<2 mEq/L) • Complete heart block with
• Widened QRS atrial asystole
complexes • At potassium
concentrations higher than
8 mEq/L, more widened
QRS complexes merge
with T waves to produce a
sine wave appearance,
which may be followed by
ventricular fibrillation and
cardiac arrest.
 CALCIUM

• Normal calcium 8.5-10.2 mg/dL

• Intracellular calcium-binding proteins include albumin, calmodulin, S100
proteins, and calcineurin.
• Albumin is the most common calcium-binding protein with clinical
relevance.  The formula for corrected calcium: Corrected calcium =
(Serum calcium + 0.8 x (4– serum albumin)
• The corrected calcium level or ionized calcium level must be used to guide
therapy, and other electrolyte disturbances (magnesium, phosphorus) must
be corrected as well. Do not replete if corrected calcium is WNL.
• Acute decrease in Mag reduces PTH  hypocalcemia (due to role in
vitamin D metabolism)
• If phosphate high, Ca combines with PO4  decreased [Ca] in blood
 HYPOCALCEMIA

Risk Factors:
• Hypoparathyroidism (s/p thyroidectomy and parathyroidectomy)
• Nutrient deficiencies (Mg, Vit D), hyperphosphatemia
• Renal or liver failure secondary to breakdown in vitamin D metabolism
• Massive transfusions
• Gastric bypass, acute pancreatitis, osteoblastic metastases
Symptoms:
• perioral numbness, tingling of the extremities, and muscle cramps.
• Acute severe hypocalcemia can result in papilledema, tetany, and seizures.
• Trousseau sign (carpopedal spasm) and Chvostek sign (facial nerve)
• ECG: prolonged QT interval
Repletion:
• Tums (calcium carbonate)
• 1-2gm calcium gluconate through PIV
• 1-2gm calcium chloride through central line
• Specific algorithms for hypocalcemia prevention and treatment after thyroid/parathyroid operations
 HYPERCALCEMIA

Risk Factors:
• Malignancy, granulomatous disorders (i.e. sarcoidosis)
• Primary and tertiary hyperparathyroidism, familial hypocalciuric hypercalcemia
• Medications (thiazides, lithium), hypervitaminosis D
Symptoms:
• Groans, bones, stones, moans, thrones, and psychic overtones
• Ca<12: maybe asymptomatic or nonspecific symptoms (fatigue, depression, constipation)
• Acute rise Ca>14: polyuria, polydipsia, dehydration, anorexia, nausea, muscle weakness, and changes in sensorium.
• ECG: QT shortened, decrease T wave flattening, ST elevation
Treatment:
• Hydration, loop diuretics, bisphosphonates, glucocorticoids, calcitonin, parathyroidectomy, dialysis
 HYPONATREMIA

• Classified as mild (130-138 mEq/L), moderate (120-130 mEq/L), or severe (<120

mEq/L)
• To diagnose, need to consider the serum osmolarity
Symptoms:
• Chronic severe, mild, and moderate hyponatremia is often asymptomatic
• Moderate to Severe hyponatremia can cause headaches and lethargy and induce
comas and seizures as cells swell due to the inability to maintain homeostatic
osmolality.
Treatment:
• Asymptomatic - Mild: raise the [Na+] by approximately 0.5mEq/h
• Symptomatic: administer sufficient Na+ as 3% NaCl until either the symptoms have
improved or the plasma [Na+] has increased by 5mEq/l, whichever comes first
• Rapid correction leads to osmotic demyelination
CAUSES OF HYPONATREMIA
 HYPONATREMIA

•  SIADH
• Inability to suppress ADH leading to unconcentrated urine
• No responsiveness to plasma osmolarity (threshold 280mosmol/kg)
• Causes increase in total body water (normal total body water volume range
is 58 ± 8% for males and 48 ± 6% for females)
• Risk Factors: drugs, CNS disturbances, malignancies, surgery, hormone
changes, HIV, hereditary, idiopathic
• Treatment: water restriction, salt tablets, loop diuretics, urea, and vasopressin
receptor antagonists (Tol/moza/sata/lixi-vaptans), democycline, lithium
• Pseudohyponatremia
• Hyperglycemia
• 1.6mEq/L for every 100mg/dL glucose (Katz)
• 2.4mEq/L for every 100mg/dL glucose (Hillier)
P.E. Watson's formula for Total Body Water
• High Protein / Gamma globulin content For males:
• Elevated lipid / triglyceride content TBW = 2.447 - 0.09156 * age + 0.1074 * height (cm) + 0.3362 * weight (kg)
For females:
TBW = -2.097 + 0.1069 * height (cm) + 0.2466 * weight (kg)
T R E AT M E N T O F H Y P O N AT R E M I A
 HYPERNATREMIA

• Hypernatremia leads to cellular shrinkage and can cause

confusion, coma, or intracranial hemorrhage.
Symptoms:
• Possibly asymptomatic at Na<160 mEq/L.
Treatment:
• Hypovolemia? Normal saline
• Free water
• dDAVP (central diabetes insipidus)
• Goal correction should be 0.5 to 1 mEq/L per hour, or 0.5
or slower in chronic situations. Overall lower to max of
10mEq/L in 24 hours.
• Rapid correction  cerebral edema
 DIABETES INSIPIDUS

• Central DI: deficiency of ADH from hypothalamus or pituitary gland

• Hypothalamic osmoreceptors, supraoptic or paraventricular nuclei, or superior portion of
supraopticophyophyseal tract
• Nephrogenic DI: resistance of ADH to kidneys
• Risk Factors:
• Usually acquired later in life, if early childhood suspect genetic
• Central: idiopathic, autoimmune process, neurosurgery, trauma, hypoxic encephalopathy, infiltrate
disorders, anorexia nervosa, post-supraventricular tachycardia
• Nephrogenic: hereditary, lithium toxicity, kidney disease, hypercalcemia, hypokalemia, drugs,
pregnancy, surgery, Bardet-Biedl, Bartter syndrome
• Treatment:
• Central: Desmopressin (dDAVP) – 2 AA substitute for ADH, potent antidiuretic without
vasopressor activity
• Nephrogenic: thiazide diuretics, NSAIDs (indomethacin > ibuprofen)
TREATMENT OF HYPERNATREMIA
 RAPID
CORRECTION
 MAGNESIUM

• Normal serum range from 1.5-2.5mEq/L, replace if low and if K is low

• Replace 2-4g magnesium sulfate IV, do not order mag citrate by accident
• Critical cofactor in ATP-powered reactions, modulates Ca, role in muscle,
insulin release
 HYPOMAGNESEMIA

Risk Factors:
• Renal losses from diuresis, tubular disease, osmotic agents, parenteral fluid therapy, and other electrolyte abnormalities.
• GI losses from chronic diarrhea or high-output ileostomy
• Skin losses from severe burn injury or toxic epidermal necrolysis
• Alcohol abuse (dietary deficiency and ETOH diuretic effect) 
• Other: catecholamine excess, pancreatitis, DM, hyperthyroidism

Symptoms:
• neuromuscular and central nervous system irritability (tremor, tetany, nystagmus, seizures, psychosis)
• Life-threatening ventricular arrhythmias (i.e. torsades de pointes)
Replacement:
• IV replacement if Mag <1 mEq/L or the patient is symptomatic
• Normal renal function, up to 2 mEq magnesium per kilogram of body weight may be administered daily. Otherwise
adjust renally.
• Treat torsades de pointes: 1 to 2 g of magnesium sulfate as an intravenous bolus during 5 minutes for treatment
(AHA and AAC).
• Oral magnesium: oxide, hydroxide, citrate, gluconate, chloride, sulfate, lactate, aspartate
• IV: Magnesium sulfate
 HYPERMAGNESEMIA

Risk Factors:
• Renal failure or metabolic acidosis
• Iatrogenic: theophylline toxicity, overdose of magnesium antacids or epsom salts, or
infusion in obstetric patients with preeclampsia or eclampsia
Symptoms:
• loss of DTRs which can progress to flaccid paralysis, apnea, heart failure, hypotension,
confusion and coma
Treatment:
• Tolerated well until >6 mEq/L
• Calcium gluconate to stabilize heart, NS for fluid expansion, and loop diuretics for renal
excretion, dialysis as last resort
 PHOSPHATE

• Normal serum range 2.5 to

4.5 mg/dL
• Most abundant intracellular
anion, only 0.1% is
extracellular
• Most important as ATP
• 85% of stores reside in bone
 strength and structure
 HYPOPHOSPHATEMIA

Risk Factors:
• Internal redistribution: insulin secretion, acute respiratory alkalosis, hungry bone syndrome, refeeding syndrome
• Decreased intestinal absorption: inadequate intake, inhibition of absorption, steatorrhea and chronic diarrhea, vitamin D deficiency or resistance,
s/p liver resection
• Increased urinary excretion: 1ry or 2ry Hyperparathyroidism, Vit D deficiency or resistance, rickets, oncogenic osteomalacia, Fanconi
syndrome, medications (acetazolamide, tenofovir, IV iron, chemo agents)
Symptoms:
• Muscle weakness
• Cardiac failure / dysrhythmias
• Respiratory failure
• Neurologic changes
• Renal and hepatic dysfunction
Replacement:
• Asymptomatic and serum 1.0-1.9 mg/dL - Oral phosphate
• P<1.0mg/dL- IV then switch to PO once P exceeds 1.5mg/dL
• PO: 1mmol/kg of elemental phosphorus given in 3-4 doses over 24 hrs
• IV dosing dependent on phosphate concentration but dangerous due to precipitation with calcium leading to kidney failure and fatal arrhythmias
 REFEEDING SYNDROME

• Potentially fatal condition occurring in patients who have experienced prolonged

periods of starvation
• Dramatic shifts of fluids and electrolytes (early) and glucose (late)
• Hallmark feature: hypophosphatemia
• Other: thiamine deficiency, hypomagnesemia, and hypokalemia
• Intracellular shifts of phosphate for ATP production
• Causes: cardiac arrhythmias, infarctions, and arrest
• Prevention:
• high potency B vitamins and daily vitamin supplementation prior to starting
enteral feedings
• 10kcal/kg/day with slow increases over 4-10 days
• Replace K, PO4, Ca, Mag and monitor until restoration of healthy body habitus
 HYPERPHOSPHATEMIA

Risk Factors:
• Renal insufficiency (w/ hypocalcemia), rhabdomyolysis
• Acute cellular shift by metabolic acidosis, tumor lysis syndrome, hemolysis
• Increased tubular reabsorption by hypoparathyroidism or pseudohypoparathyroidism, acromegaly
• Bisphosphonates, FGFR inhibitors, vitamin D toxicity, phosphate-containing laxatives

Symptoms:
• Typically asymptomatic
• S/Sx from (1) the effects of hypocalcemia, such as muscle cramps, tetany, and perioral numbness or tingling,
or (2) underlying uremic symptoms, such as fatigue, shortness of breath, anorexia, nausea, vomiting, and
sleep disturbances. 
Treatment:
• Saline infusion (can worsen hypocalcemia)
• Acetazolamide at 10 to 15 mg/kg every 3 to 4 hours
QUESTIONS
A 25-year-old man, who had a total thyroidectomy 3 days ago, presents to the emergency
department with painful cramping in his hands. On examination, you find that his hands appear
to be locked in a flexed position. The corrected serum calcium level is 7.0 mg/dL. What is the
best course of immediate action?

A. Serum parathyroid hormone levels

B. Serum magnesium levels
C. Infusion of 2g of intravenous calcium gluconate
D. Administration of oral calcitriol
E. Infusion of IV calcium chloride
 ANSWER IS C

• Given the fact that this patient is presenting with tetany, intravenous calcium is the most
important next step. Calcium gluconate is safe to infuse through a peripheral intravenous line and
is highly effective at quickly alleviating symptoms. This patient will likely need to be on an oral
calcium/calcitriol regimen that should be slowly tapered.Parathyroid hormone levels will almost
certainly be low after thyroidectomy, but details about values will not address the hypocalcemia
or provide any more information. It is necessary to correct any magnesium abnormalities, but this
is not the most important course of action given the severity of the patient's symptoms. Calcitriol
is the most bioavailable form of vitamin D and would help with the absorption of any
supplemental calcium that is given to this patient. However, the first course of action in the
presence of tetany is intravenous calcium. Calcium chloride is corrosive to veins and must be
administered through a central vein. This patient has tetany and does require immediate
intravenous calcium, but calcium gluconate is a better option in this setting to avoid the
morbidity of an unnecessary central line.
An 80-year-old man is in the intensive care unit with multiple injuries after a motor vehicle crash 2 weeks ago.
He is currently receiving intravenous heparin for a recently diagnosed pulmonary embolism. Bilateral lower
extremity ultrasound done in the last 24 hours demonstrate no evidence of DVT. He suddenly becomes
hypotensive and is unresponsive to boluses of normal saline and a Dopamine infusion. Electrolytes measured 24
hours ago were normal and the hemoglobin was 11.9 g/dL. Laboratory studies reveal sodium 120 mEq/L,
potassium 6.0 mEq/L, bicarbonate 16 mEq/L, blood urea nitrogen 10 mg/dL, creatinine 1.0 mg/dL, and glucose
110 mg/dL. What is the most appropriate next step in treatment?

A. Give a 2 L bolus of 5% dextrose normal saline

B. Start a norepinephrine infusion
C. Give hydrocortisone 100 mg IV
D. Initiate 3% NaCl infusion through central access
E. Give calcium gluconate injection
 ANSWER IS C

• The constellation of hypotension unresponsive to fluid resuscitation with

hyponatremia, hyperkalemia, and a non–anion gap metabolic acidosis suggests
Addisonian crisis. It is likely the result of heparin-induced adrenal hemorrhage.
Immediate replacement with an intravenous corticosteroid is life-saving;
mortality from this condition remains high if there is delay in initiating steroid
treatment. If intravenous access is not available, it should be given by the
intramuscular route. Supportive treatment with fluids, pressors, and electrolyte
replacement should be done after giving steroids.
A 45-year-old woman is brought to the emergency department with weakness and dizziness. She has a history
of hypertension and end-stage renal disease. Her blood pressure is 90/55 mm Hg and her pulse is 45
beats/min. Physical examination shows significant muscle weakness and absent deep tendon reflexes. It is
learned that she missed both of her last dialysis appointments. Which of the following electrolyte
abnormalities is most likely causing the patient's symptoms?

A. Hypomagnesemia
B. Hypermagnesemia
C. Hypokalemia
D. Hyperkalemia
E. Hypophosphatemia
 ANSWER IS B

• End-stage renal disease can cause decrease excretion of magnesium. The patient
also missed two dialysis appointments, which would have helped lower the
magnesium level. The patient is exhibiting symptoms of hypermagnesemia.
Severe hypermagnesemia can lead to electrocardiographic changes and cardiac
arrest. Treatment involves calcium gluconate, diuresis, and dialysis.
Hypomagnesemia is often hidden by concurrent hypokalemia and hypocalcemia.
Symptoms may include hyperreflexia, tremor, Trousseau sign, Chvostek sign,
along with vague symptoms such as nausea, vomiting, and weakness.
A 56-year-old man with a history of obesity, hyperlipidemia, essential hypertension, gastroesophageal reflux disease,
and major depression presents to his primary care physician’s clinic for his annual visit. He has no complaints at this
time. He takes simvastatin, atenolol, lisinopril, pantoprazole, and escitalopram. Laboratory tests show low magnesium
and calcium. What drug might be causing this electrolyte imbalance?

A. Simvastatin
B. Atenolol
C. Lisinopril
D. Pantoprazole
E. Escitalopram
 ANSWER IS D

• Pantoprazole is a proton-pump inhibitor (PPI). A risk factor for hypomagnesemia is

chronic PPI use. Hypocalcemia can develop as hypomagnesemia progresses;
magnesium is a cofactor for parathyriod hormone. Mild hypomagnesemia can present as
asymptomatically, vague general symptoms, such as nausea, vomiting, weakness or as
hypocalcemia with Trousseau sign, Chvostek sign, hyperreflexia, and tremor. Severe
hypomagnesemia of less than 1 mg/dL can lead to a generalized tonic-clonic
seizure. Medications that can cause hypomagnesemia include proton pump inhibitors;
diuretics, both loop and thiazide, amphotericin B; and cisplatin. Gastrointestinal disease,
chronic diarrhea, and alcohol use disorder can also lead to low levels of magnesium.
A 32-year-old woman with known bipolar disorder with schizophrenic features is found to have a sodium level
of 124 mEq/L and presents to your office with confusion. Two months ago, the patient's sodium level was
normal. Your working diagnosis is psychogenic polydipsia versus syndrome of inappropriate antidiuretic
hormone (SIADH). Which labs and studies will differentiate between these two conditions?

A. Serum Na and serum osmolarity

B. Serum Na and urine osmolarity
C. Urine Na, serum osmolarity and urine osmolarity
D. Urine Na, urine osmolarity, and serum K
 ANSWER IS C

• SIADH and psychogenic polydipsia often present in very similar fashions.

Both have hyponatremia as their main feature, and both have low serum
osmolarity. To differentiate between the two, urine sodium and urine
osmolarity are crucial studies to obtain. In SIADH, the urine osmolarity and
urine sodium will be elevated, as antidiuretic hormone will inappropriately
work on the distal collecting system. In psychogenic polydipsia, the urine
sodium and urine osmolarity will be maximally low as the body appropriately
tries to keep sodium.
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