Step Up - Fluids and Electrolytes

Question 1

Describe the distribution of fluid in the body in terms of ICF, ECF, plasma, and interstitial fluid.

Answer 1

1) ICF - 2/3 of TBW
2) ECF - 1/3 of TBW
a) Plasma 1/3 of ECF
b) Interstitial fluid 2/3 of ECF

Question 2

What is the best way of assessing volume status? What is expected? What else can be used to assess volume status?

Answer 2

1) Urine output 0.5-1.0ml/kg/hr in adults
2) Clinical picture is important
a) burns, fever, open wounds lead to greater insensible losses
b) Patients with liver failure, nephrotic syndrome, CHF, hypoalbuminemia third-space and are intravascularly deplete despite normal TBW
c) ESRD leads to hypervolemia

Question 3

What are the causes of hypovolemia (5)?

Answer 3

GI loss (vomiting, diarrhea, NG suction)
third-spacing (ascites, effusions)
Low intake
Polyuria (DKA)
Sepsis and inflamatory processes
Trauma, open-wounds, burns
Insensible losses - diaphoresis, tachypnea

Question 4

What are the clinical features of hypovolemia (5)?

Answer 4

1) CNS deficits - mental status change, sleepiness, apathy, coma
2) CV findings - orthostatic hypotension, tachycardia, low pulse pressure, decreased CVP
3) Skin change - poor turgor, cold, pale
4) Oliguria
5) Ileus, weakness
6) AKI - azotemia

Question 5

What is the rule for calculating maintenance fluids? What is typically used for maintenance fluid?

Answer 5

1) 4//2/1 - 4ml/kg first 10kg, 2ml/kg second 10kg, 1ml/kg for weight over 20kg (gives 110ml/hr for 70kg person).
2) D51/2NS with 20mEq/L KCL

Question 6

What are the causes of hypervolemia (2)? What are the clinical features (5)? How is it treated (2)?

Answer 6

1) Causes: iatrogenic, fluid-retaining states (CHF, nephrotic syndrome, cirrhosis, ESRD)
2) Clinically: wt gain, peripheral edema/ascites/pulm edema, JVP elevated, High CVP, pulmonary rales, low hematocrit
3) Tx: fluid restrict, diuretics

Question 7

What does hyper/hyponatremia represent? What does hyper/hypovolemia represent?

Answer 7

1) Too much or too little WATER

2) Too much or too little NA

Question 8

Where does furosemide work in the kidney and what does it impair? Where do thiazides work in the kidney, what does it impair?

Answer 8

1) Furosemide - works on ascending loop, blocks Na/Cl/K transporter
2) Thiazides - works on early distal tubule, blocks Na/Cl transporter.

Question 9

`How is serum osmolality calculated?

Answer 9

Sosmo = 2Na + Urea + Glc (all in mmol/L)

Question 10

What is the first step in the work-up of hyponatremia? Briefly describe each category.

Answer 10

Check serum osmolality and classify hyponatremia as follows:

1) Osmo > 295: hypertonic hyponatremia (osmotic substances present - hyperglycemia, mannitol, glycerol)
2) Osmo 280-295: isotonic hyponatremia (pseudohyponatremia, increased plasma solids such as proteins or TGs)
3) Osmo less than 280: hypotonic hyponatremia - this is true hyponatremia

Question 11

How is hypotonic hyponatremia further subclassified (3)? What are the causes of each?

Answer 11

1) Hypovolemic:
a) Low urine sodium: extrarenal losses (diarrhea, vomiting, diaphoresis, third-spacing, burns)
b) High urine sodium: renal losses (ATN, diuretics, low aldosterone (ACEi)).
2) Euvolemic: SIADH, psychogenic polydipsia, hypothyroidism, oxytocin use, excess free water administration, drugs (haldol)
3) Hypervolemic: water retaining states with more water than sodium retained. Cause: CHF, nephrotic syndrome, liver disease

Question 12

What are the clinical features of hyponatremia (5)?

Answer 12

1) Neuro findings - cerebral edema, headache, delirium, irritability, muscle twitching, weakness, hyperactive DTR
2) Increased ICP - seizures, coma
3) GI - N/V, ileus, watery diarrhea
4) CV - hypertension 2nd to high ICP
5) Increased sallvation and lacrimation
6) Oliguria

Question 13

Will the urine osmolality be high or low in true hyponatremia?

Answer 13

Depends on cause:

1) If kidneys are responding properly, then osmolality is low (dilute urine). Ex. primary polydipsia
2) Osmolality high if high ADH. Ex. CHF, SIADH

Question 14

How is true hyponatremia treated (hypotonic hyponatremia)?

Answer 14

1) Mild (Na 120-130): water restrict
2) Moderate (Na 110-120): loop diuretics and saline (to prevent ADH activation)
3) Severe (under 110): hypertonic saline to correct
- Do not correct by more than 8mmol/L in 24hrs.

Question 15

What is the first step in working-up hypernatremia? How is hypernatremia classified? What are the causes of each type?

Answer 15

1) Assess clinical ECF volume
2) types:
a) Hypovolemic hypernatremia
- low Na and low water (more so)
- Renal loss: diuretics, osmotic diuresis (glucose), renal failure
- Extrarenal loss: diarrhea, diaphoresis, respiratory
b) Euvolemic hypernatremia
- normal Na, low water
- DI, insensible respiratory (tachypnea)
c) Hypervolemic hypernatrmia
- Gain of water and gain of Na (more so)
- Iatrogenic (TPN, NaHCO3), exogenous glucocorticoids, cushing’s syndrome
- rare.

Question 16

What are the clinical features of hypernatremia? How is each type treated?

Answer 16

1) Neurological findings - altered mental status, restless, weak, confusion, seizure, coma. Mucous membranes dry
2) Treatment
a) Hypovolemic - give isotonic NaCl to restore volume, replace free water deficit later
b) Euvolemic - Vasopressin for DI. Oral fluids
c) Hypervolemic - diuretics (furosemide) and D5W to replace water deficit

Question 17

What are the causes of hypocalcemia (5)? What are the clinical features (5)? How is it treated?

Answer 17

1) Causes: hypoparathyroidism, acute pancreatitis, renal insufficiency (low vit D), hyperphosphatemia, pseudohypoparathyroidism, hypomagnesemia, vit D def, malabsorption
2) Clinical: can be asymptomatic, rickets/osteomalacia, neuromuscular irritability (brisk DTR, Chvostek sign, Trousseau sign), basal ganglia calcifications, Cardiac (prolonged QT and arrhythmias)
3) Tx: treat underlying cause

Question 18

Comment on the serum Phos and PTH in the following causes of hypocalcemia: hypoparathyroidism, vitamin D deficiency, pseudohypoparathyroidism

Answer 18

1) Hypoparathyroidism: high phos, low PTH
2) Vitamin D def: low phos, high PTH
3) Psuedohypoparathyroidism: - , very high PTH

Question 19

What are the causes of hypercalcemia (5)? What are the clinical features (5)?

Answer 19

1) Causes:
a) Endo - hyperparathyroidism, Paget’s, acromegaly
b) Malignancies - metastatic, multiple myeloma, tumors that secrete PTH-like hormone
c) Pharma - vit D intoxication, milk, thiazide diuretics
2) Clinical
a) Stones
b) Bones - bone pain
c) Groans - muscle pain, pancreatitis, gout
d) Psych overtones - depression, fatigue, anorexia
e) Other - HTN, wt loss, shortened QT

Question 20

How is hypercalcemia treated (4)?

Answer 20

1) IV fluids and loop diuretics
2) Inhibit bone resorption in malignancy - bisphosphonates
3) Glucocorticoids if vit D-related mechanism
4) Hemodialysis if renal failure.

Question 21

Provide a differential diagnosis for hypokalemia.

Answer 21

1) Redistributive - insulin excess, metabolic alkalosis, epinephrine
2) Renal loss - RTA, DKA, ureterosigmoidostomy
3) Extra-renal losses - low intake, laxative abuse, perspiration, diarrhea, fistula
4) Spurious - lab error

Question 22

What are the clinical features of hypokalemia (5)? How is it treated (3)?

Answer 22

1) Clinical: arrhythmias, muscle weakness, low DTR, paralytic ileus, flat T waves with U-waves
2) Tx:
a) Oral or IV K - 10mEq corrects by 0.1
b) IV infusion rate no more than 10mEq/hr
c) Correct Mg deficit if present

Question 23

What are the causes of hyperkalemia (5)?

Answer 23

1) Redistribution - acidosis, insulin deficiency, B-blockers
2) Renal failure
3) Renal impairment
a) Low aldosterone - ACEi, Addison’s disease
b) N or high aldosterone - potassium sparing diuretics, tubular disorders
4) Spurious - lab error, hemolysis

Question 24

What are the clinical features of hyperkalemia (5)? How is it treated (4)?

Answer 24

1) Clinical: arrhythmias - peak T waves, widened QRD, PR prolongation, loss of P waves, VFib. Muscle weakness, low DTR, resp failure
2) Tx (severe): IV calcium, glucose and insulin or bicarb to shift K into cells, remove K with Kayexalate, dialysis, or diuretics

Question 25

Provide a differential for AG metabolic acidosis (4).

Answer 25

1) Ketoacidosis - Dm, prolonged starvation, prolonged alcohol abuse
2) Lactic acidosis - low perfussion, shock states
3) Renal failure - low NH4 excretion
4) Intoxication - salicylate, methanol, ethylene glycol

Question 26

Provide a differential for non-AG metabolic acidosis (2)/

Answer 26

1) Renal loss of bicard - prox or distal tubule acidosis

2) GI loss of HCO3

Question 27

What is the anticipated PaCO2 response to a metabolic acidosis (Winter’s formula)?

Answer 27

expect that PaCO2 = 1.5*HCO3 + 8 +or-2

• if response appropriate, then met acidosis
• if response to little, then met acidosis and resp acidossis
• if response to high, then met acidosis, and resp alk

Question 28

Describe the 2 categories of metabolic alkalosis and what causes each.

Answer 28

1) Saline-sensitive met alk
a) Ucl less than 10
b) Cause: ECF contraction (diuretics) or H loss with vomiting
c) Tx: Saline
2) Saline-resistant met alk
a) Ucl > 10, hypervolemic
b) Cause: adrenal disorders (primary hyperaldosteronism)
c) Tx underlying cause

Question 29

What is the renal adaptation to a respiratory acidosis in terms of adjustment to HCO3 for every 10mmHG increase in PCO2

Answer 29

Anticipate HCO3 increase of 4mmol/L (in chronic setting)