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Electrolytes and Friends

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aliasesLabs, labs

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Potassium

Hypokalemia:

Much more well tolerated than hyperkalemia

  • Main causes: GI losses, Renal Losses, Intracellular shifts, Low K Intake
    • GI Losses: Diarrhea, vomiting, NG tube, etc.
    • Renal losses: diuretics, nephrotic syndrome, etc
    • Intracellular shifts: medications (insulin, beta agonists, etc)
    • Low K intake: rare, alcoholics/anorexia
      Potassium Repletion
  • LOOK AT PHOSPHORUS
  • 3<K<3.5 and asymptomatic: oral (if able)
  • <3.0: IV potassium
  • K goes up .1 every 10 meq
  • Max repletion rate: 1 meq /kg / day
  • How to order: e.g. 10 meq in 50mL ran over 1 hour (times how much K needs to increase)
    • PIV: 10meq/hr
    • Central line: 20meq / hr
  • IV potassium burns veins

Hyperkalemia:

  • Main causes: hemolysis of lab sample, acidosis, medications, decreased renal excretion, excessive intake
    • Hemolysis: always ask “does this make sense”
    • Acidosis: pH<7.35 causes shift extracellular
    • Meds/Decreased renal excretion: ACE-I, MRA, Beta Blockers, AKI/CKD
    • Excessive intake: ate too much! Rare

Total Bilirubin / AST / ALT / ALP / GGT :

Important functional measures of hepatobiliary system

Patterns:
R Factor for Liver Injury = points towards cholestatic vs. hepatocellular vs mixed injury
Cholestatic

  • increased ALP and GGT
    Mixed:
  • increased AST/ALT and ALP
  • think DILI, late viral hepatitis, early biliary obstruction
    Hepatocellular:
  • viral/autoimmune hepatitis, hemochromatosis, Wilson’s disease, alpha 1 antitrypsin deficiency
  • AST predominant: alcohol / cirrhosis

Bilirubin

Elevated bilirubin should be fractionated to indirect (unconjugated) and direct (conjugated)
Abnormal concentrations may indicate cholestasis or hepatocellular damage in the presence of other abnormal liver tests

  • Jaundice = Tbili > 2.5-3.5
  • Direct = conjugated
  • Conjugated bili = pruritis
    Vocab:
  • kernicterus (bilirubin encephalopathy) - brain damage causes by newborn bilirubin buildup
    • unconjugated bili > 25

AST / ALT

  • markers of hepatocellular injury
  • ALT more specific to liver
  • Generally, hepatocellular injury results in an AST:ALT ratio >1. However, alcoholic liver disease usually presents with a ratio of ≥2. This ratio may also be elevated in cases of NAFLD, cirrhosis, or Wilson disease, but the elevation is usually not >2

Clinically significant elevations:
The American College of Gastroenterology defines the following categories for AST and ALT elevations:
• Borderline: <2× ULN
• Mild: 2–5× ULN
• Moderate: 5–15× ULN
• Severe: >15× ULN
• Massive: >10,000 IU/L

Borderline and mild elevations (<5× ULN) are most commonly seen in metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD), alcoholic liver disease, chronic viral hepatitis, and drug-induced liver injury. 

Moderate elevations (5–15× ULN) may be seen in acute viral hepatitis, drug-induced liver injury, or autoimmune hepatitis. 

Severe and massive elevations (>15× ULN, especially >10,000 IU/L) are typically associated with ischemic hepatitis (shock liver), severe drug-induced/toxic hepatitis (e.g., acetaminophen toxicity), or acute viral hepatitis. Non-hepatic causes such as rhabdomyolysis can also result in very high AST levels.

Alk Phos / GGT

Elevation of ALP is suggestive of cholestasis
Serum 1/2 life: 7 days

  • can take 1 week to decrease following resolution of biliary obstruction
    GGT and/or 5’NT may be useful to identify whether ALP elevation has a hepatic origin
    ALP also found in:
    1. Liver
    2. Bone
    3. Kidney
    4. Intestine
    5. Neutrophils
      GGT:
  • GGT measurement can be used to confirm the origin of elevated ALP
  • Elevated GGT indicates a hepatic cause of ALP elevation
  • GGT is often used to evaluate alcohol use, but it is nonspecific and may be elevated with diseases such as NAFLD and other hepatobiliary disorders
Causes of elevated ALP
  1. Biliary obstruction (intra/extra hepatic)
  2. Other liver pathologies: cancer, DILI, infections, etc
  3. Cancer
  4. Pregnancy (fetal isoenzyme)
  5. AIDS
  6. Other: intra-abdominal infections, cholestasis of sepsis, Hodgkin lymphoma, myeloid metaplasia, and osteomyelitis
  7. Leukemoid reaction

Synthetic Function

Albumin

  • Liver disease decreases albumin synthesis and decreases serum albumin concentration
  • In the absence of other markers of liver disease, low albumin concentration may be related to malnutrition or protein loss (e.g., malabsorption)

PT:

  • Elevated PT that is unresponsive to vitamin K supplementation is suggestive of poor liver function

Calcium:

general

total calcium is a screening test only -  ionized calcium is what matters physiologically

  • 8.5-10.5 mg/dL (or 2.12-2.62 mM) is the normal range.
    • Total calcium is not an accurate predictor of ionized calcium (since ionized calcium depends on numerous factors including pH, albumin level, sodium level, and phosphate level).
  • iCal measures the biologically active calcium. This is the most accurate and preferred way to measure calcium.
    • 1.1-1.3 mM is the normal range seen in healthy people, but most critically ill patients tend to run below this range.
    • <0.8 mM probably warrants treatment (although there is no clear evidence that treatment improves outcomes).
    • <0.65 mM is critically low (possibly causing hypotension)

Serum calcium = ionized calcium + bound calcium (albumin)
Interpret # in context of albumin

  • basically impossible to be hypocalcemic if you have bones and a working PTH axis
  • HOWEVER:
    • Ca is albumin bound
    • low albumin = low total calcium (but not functional aka ionized Ca)

ST segment duration is inversely related to the ionized calcium level

  • Hypercalcemia causes ST segment shortening
  • Hypocalcemia causes ST segment prolongation.
  • This may be noticed as QT prolongation with a normal-sized T-wave.
    • This may be seen on the patient’s monitor or on a rhythm strip (without a full EKG).
  • Hypocalcemia may cause torsade de pointes.

Hypocalcemia:

Causes:

  • hypoparathyroidism
  • impaired vitamin d synthesis / action
    • inadequate intake
    • malabsorption
    • liver disease / CKD
    • hypomagnesemia
  • calcium chelation / precipitation
    • Hyperphosphatemia of any etiology, for example:
    • Renal failure.
    • Tumor lysis syndrome.
    • Rhabdomyolysis.
  • Exogenous citrate:
    • Massive transfusion (especially if combined with hepatic/renal dysfunction).
    • Plasmapheresis and leukapheresis (fresh frozen plasma contains citrate).
    • Renal replacement therapy with citrate regional anticoagulation.
  • Pancreatitis (may relate to systemic inflammation and release of free fatty acids).
  • Poisoning:
    • Ethylene glycol poisoning
    • Hydrofluoric acid.
      Chvostok’s Sign:
      Trousseau Sign:  inflate a blood pressure cuff to 20 mm Hg above the systolic blood pressure for 3 minutes to elicit carpal spasms because of the increased excitability caused by local ulnar and median nerve ischemia.

Albumin:

Important synthetic measure of liver - is the liver producing the things it’s supposed to?
(Note- clotting factors/fibrinogen are often preserved or even increased in low albumin states)

Causes of low albumin:

  • #1: infection/inflammation (negative acute phase reactant)
  • CKD / nephrotic syndrome (>3.5g / day)
  • Damaged liver (cirrhosis, hepatitis, surgical resection, etc)
  • Malnutrition

Sodium:

Hyponatremia

  • MC is hypotonic (90%)
  • MC Cause inpatient: fluids (iatrogenic hypervolemic hyponatremia)
    • Urine Studies:
      • uOsm: >100= ADH is working, <100= ADH is not working
      • uNa: <20=kidneys are working, >20=kidneys are losing Na
  • Hypotonic Hyponatremia: 90% of cases
    • Hypovolemic:
      • GI losses, 3rd spacing, Diuretic meds
        • uNa<20: GI losses, 3rd spacing
        • uNa>20: Diuretic meds
    • Euvolemic:
      • SIADH
        • uOsm>100: SIADH, hypothyroidism, Adrenal insufficiency
        • uOsm<100: “tea and toast” diet, beer potomania, primary polydipsia
    • Hypervolemic:
      • CHF, cirrhosis, renal failure
        • uNa<20: CHF, cirrhosis
        • uNa>20: Renal failure
    • Treatments:
      • Hypovolemic: Fluids (NS)
      • Euvolemic: Fluid Restriction
      • Hypervolemic: Diuresis

Hypernatremia

  • Free Water Deficit
  • AI/DI

Hemoglobin:

  • RBC life = 120 days
  • Rapid changes = bleeding or hemoconcentration/dilution
    • Do you suspect bleeding?
      • Look for signs in foley, drain, poop, vomit, POCUS, etc
    • Cross reference with fluid administration and urine/drain output
      • Changes in Hgb concordant with volume status = likely not bleeding
  • Urine Output
    • Weight (kg) x 0.5 = mL/hr
    • Average adult: 30mL/hr or 720mL/day
    • 1L/day = 42mL/hr = 84kg patient (185lbs)

Creatinine:

  • complete anuria will raise Cr by 1.0 mg/dl per day
  • not elevated until ~%50 reduction in renal function
  • KDIGO

BUN

  • End product of protein metabolism
  • 85% eliminated by kidneys, 15% by GI tract
  • Increases if renal elimination impaired (AKI, CKD), GI bleeding, high protein diet, severe liver disease
  • Increases earlier in chronic renal dysfunction than SCr

Ammonia

Hepatic Encephalopathy

  • not indiciative of degree of encephalopathy

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