Fluid and Electrolytes

 

I.                    Total Body Water (TBW): 60% of weight in men, 50-55% in women

a.       Intracellular: 2/3rds of TBW

b.      Extracellular: 1/3rd of TBW

                                                               i.      Interstitial space: 3/4ths of extracellular; 16% TBW

                                                             ii.      Vascular: 1/4th extracellular, 4% TBW

                                                            iii.      Osmolarity: 2 x [Na] + (glucose/18) + [BUN]/2.8 ~ 290mOsm

II.                 Fluid Balance

a.       Normal: 30ml/kg/day of water lost through urine (15ml), stool (3ml), sweat (0-1.5ml) and lungs/skin (10ml).

b.      Abnormal:

                                                               i.      Require 500ml more if febrile; give hypotonic replacement

                                                             ii.      Abdominal and thoracic surgery requires 1,000ml replacement by LR or normal saline to replace 3rd spacing

                                                            iii.      3rd spacing resolves on POD #3 and later

                                                           iv.      TPN causes osmotic diuresis; don’t confuse high urine output with high fluid status

III.               Volume Depletion

a.       Clinical diagnosis:

                                                               i.      1st signs: skin turgor, dry mucous membranes, oliguria

                                                             ii.      later signs: mental status changes

b.      Treatment: give fluids

                                                               i.      LR for most causes of isotonic losses (intestinal, biliary, pancreatic, 3rd spacing)

                                                             ii.      Gastric losses best treated with isotonic crystalloid; LR has inadequate Cl to deal with hypochloric, hypokalemic metabolic alkalosis of persistent vomiting

                                                            iii.      Glucose solutions not a good idea for volume replacement: can cause osmotic diuresis if too much is given

IV.              Volume Overload

a.       Almost always iatrogenic (gave the wrong kind of fluids, like hypotonic solution for gastric losses)

b.      Sequellae: ranges from weight gain and hemodiluation to CHF and pulmonary edema

c.       Treatment: fluid restriction for mild cases, loop diuretics for severe cases

V.                 Prerenal azotemia:

a.       urine Na <20mEq/L

b.      BUN:Creatinine > 20:1

c.       Urine osmolality > 400mOsm/L

VI.              Acute renal injury

a.       Urine Na >40mEq/L

b.      BUN:Cr < 10:1

c.       Urine osm ~ plasma osm (kidneys can’t concentrate)

VII.            Sodium balance:

a.       aldosterone stimulated by extracellular volume reduction via renin; also by increased K and ACTH

b.      ADH: osmole receptors in brain trigger its release when blood is too concentrated; volume dominates over osmolar if in conflict

c.       Hyponatremia: says nothing about volume status

                                                               i.      Dilutional: common in surgical patients as 1ml free water is produced with catabolic breakdown of 1 gram of fat or muscle

                                                             ii.      Clinical: Na <130 causes irritability, weakness, fatigue, increased reflexes, muscle twitches; <120 causes seizures and coma

VIII.         Potassium balance:

                                                               i.      excretion directly related to aldosterone and intra- and extracellular K levels

                                                             ii.      affected by acid-base status: acidoses causes hyperK, alkalosis causes hypoK

b.      Hypokalemia

                                                               i.      Look for concurrently low levels of Mg, Ca and phosphorous

                                                             ii.      K lost through GI tract

1.      highest conc of K found in colon and rectum

2.      NG sucks out K; loss of HCl also creates alkalosis which puts K into the tissues in exchange for H; kidney then saves H by excreting K

                                                            iii.      aldosterone causes K loss from kidneys until K levels too low – then paradoxical aciduria is formed as kidney lose H to save K even though blood is alkalotic

                                                           iv.      Renal loses of K

1.      iatrogenic: loop diuretics

2.      low Mg causes low K resorption in distal loop (unknown mechanism)

                                                             v.      Clinical manifestations (only seen when serum K is <3.0)

1.      weakness, absent reflexes

2.      increased ammonia production worsens hepatic encephalopathy

3.      cardiac: flattened T-waves, U waves, depressed S-T, prolonged P-R, widened QRS

4.      Watch for digoxin toxicity

                                                           vi.      Treatment: replace K and fix underlying problem

1.      Don’t exceed 10mEq/hr IV (unless you want to watch how the death penalty is carried out via lethal injection)

2.      Don’t give with dextrose; increased insulin will hide K in cells making serum levels harder to elevate

c.       Hyperkalemia

                                                               i.      Causes:

1.      Endogenous causes: cell lysis, rapid catabolism of fat and muscle, renal insufficiency

2.      Iatrogenic: K sparing diuretics, NSAIDS, ACE inhibitors

                                                             ii.      Clinical manifestations:

1.      peripheral weakness leading to respiratory paralysis

2.      Cardiac: peaked T waves, flattened P waves, increased P-R interval, decreased Q-T, widened QRS, sine waves, v fib, flat line

                                                            iii.      Treatment: restrict intake, give insulin, K-Dur resin to pull it out the GI tract, IV calcium gluconate to protect heart, dialysis for renal failure

d.      Chloride

                                                               i.      Hypochloremia

1.      Cl lost to NG tube

2.      Will impair kidney’s ability to recover from respiratory acidosis (kidney corrects by holding onto bicarb, but needs Cl to secrete bicarb when acidosis is resolving, thus metabolic alkalosis results)

3.      Treated with NaCl and KCl in appropriate ratio

                                                             ii.      Hyperchloremia

1.      Iatrogenic cause is diversion of urine into the bowel: bicarb exchanged for Cl in the urine

2.      No specific treatment for hyperCl

e.       Calcium: regulated by PTH and Vitamin D

                                                               i.      Hypocalcemia

1.      seen in acute pancreatitis; also low Mg blocks release of PTH; high phosphate causes bones to absorb Ca

2.      severe soft tissue infections cause low Ca too

3.      Clinical: tingling, numbness, hyperactive reflexes, Chvostek sign (facial twitch upon tapping), mental status change

4.      Treatment: calcium gluconate or calcium chloride via IV

                                                             ii.      HyperCa

1.      Causes: hyperparathyroid and metastatic breast cancer (secrete PTH-like substances); milk-alkali: excessive intake of calcium and absorbable antacids

2.      Clinical:

a.       weakness, anorexia, vomiting, headaches, mental status change

b.      Cardiac: shortened Q-T, widened T-waves

3.      Treatment: restrict Ca intake, IV fluids, loop diuretics, IV phosphate to bind Ca, corticosteroids to reduce bone release in patients with granulomatous disease, plicamycin reduces serum Ca in mysterious ways

f.        Magnesium

                                                               i.      Low magnesium causes low potassium and phosphate; also low calcium by blocking PTH release

1.      clinically looks like low calcium

                                                             ii.      high magnesium seen often in renal failure and muscle damage; also eclampsia treatment causes it

1.      clinically causes nausia, weakness, decreased reflexes; hypotension and bradycardia are late signs

g.       Phosphate

                                                               i.      Low phosphate seen in chronic EtOH abuse and lots of other things

                                                             ii.      High phosphate can be from sarcoid or TB; symptomless

IX.              Acid-Base disturbances: if these concepts weren’t pounded into you during the Renal committee, there’s really no hope for you now