Laboratory Abnormalities

This guide provides evidence-based approaches to diagnosing and managing common laboratory derangements encountered in internal medicine practice.

Electrolyte Replacement Protocols

Potassium Repletion

Potassium supplementation depends on the serum level and patient factors. Always consider renal function before aggressively replacing.

Serum K+ (mEq/L)	Oral Replacement	IV Replacement	Frequency
3.6-3.8	40 mEq	20 mEq	Once
3.3-3.5	40 mEq	20 mEq	Every 2-4 hours, twice total
2.8-3.2	40 mEq	20 mEq	Every 2-4 hours, three times total
<2.8	40 mEq	20 mEq	Every 2-4 hours, three times + additional IV support

Caution in Renal Disease

Patients with end-stage renal disease, chronic kidney disease, or acute kidney injury have impaired urinary potassium excretion. Use significantly less aggressive replacement strategies to avoid hyperkalemia. Consider nephrology consultation if K+ <2.8 in these populations.

Clinical Pearls - Potassium

Approximately 10 mEq of potassium raises serum concentration by 0.1 mEq/L
Oral and intravenous replacement have equivalent efficacy
Magnesium depletion causes increased urinary potassium wasting—always check and correct magnesium concurrently
Recheck serum levels approximately 2 hours after completing supplementation
Low magnesium levels (<1.6 mEq/L) perpetuate hypokalemia and should be repleted first

Magnesium Repletion

Magnesium supplementation is essential when levels fall below normal, as hypomagnesemia impairs the kidney's ability to retain potassium.

Serum Mg (mg/dL)	IV MgSO4 Dose	Infusion Duration	Notes
1.8-2.0	1 g	2 hours	Gradual replacement
1.6-1.7	2 g	2 hours	Moderate depletion
<1.5	2 g	2 hours	Severe depletion; may require repeat dosing

Magnesium Replacement Calculation

Each 1 gram of magnesium sulfate administered intravenously raises serum magnesium concentration by approximately 0.1 mg/dL. Monitor and recheck levels after completing infusion.

Phosphorus Repletion

Phosphate supplementation addresses severe hypophosphatemia. Choose the salt based on concurrent sodium and potassium status.

Serum PO4 (mg/dL)	Sodium Phosphate Dose	Infusion Duration	Clinical Approach
2.0-2.4	15 mmol	4 hours	Mild depletion; slower infusion acceptable
1.0-1.9	30 mmol	4 hours	Moderate depletion
<1.0	45 mmol	4 hours	Severe depletion; monitor closely

Potassium Phosphate Considerations

Use potassium phosphate for oral replacement when serum phosphate is >2 mg/dL or if sodium is elevated
Each mmol of potassium phosphate contains 1.5 mEq of potassium—account for this when calculating total daily potassium load
Monitor serum sodium and potassium carefully when using potassium phosphate preparations

Hyponatremia (Serum Sodium <135 mEq/L)

Hyponatremia results from excess total body water relative to sodium. The workup follows a systematic approach: establish true hyponatremia, determine volume status, and identify the underlying cause.

Initial Workup

Begin by measuring three key parameters:

Serum osmolality (measured or calculated)
Urine osmolality
Urine sodium concentration

Normal reference values: Urine sodium ~20 mEq/L, Urine osmolality 50-1200 mOsm/kg, Serum osmolality 280-303 mOsm/kg

Step 1: Confirm True Hyponatremia

Calculate serum osmolality using the formula:

Serum Osmolality = 2×(Na + K) + (Glucose ÷ 18) + (BUN ÷ 2.8)

Compare calculated osmolality to the measured value to classify the hyponatremia:

Hypertonic (Pseudohyponatremia)

Measured osmolality > Calculated osmolality

Occurs when the serum contains unmeasured osmotically active particles. Serum sodium appears low but tonicity is normal.

Hyperglycemia: Each 100 mg/dL of glucose above 100 requires correction using: Corrected Na = Measured Na × 1.6
Toxic ingestions: Methanol, ethylene glycol, propofol
Hypertriglyceridemia or hyperproteinemia: Laboratory artifact from laboratory analysis technique

Isotonic (Pseudohyponatremia)

Measured osmolality ≈ Calculated osmolality

Serum osmolality is normal despite low reported sodium value. This is a laboratory error from elevated lipids or proteins that displace the aqueous phase.

Hypotonic (True Hyponatremia)

Measured osmolality < Calculated osmolality

Genuine hyponatremia with decreased serum tonicity. This is the form requiring treatment. Proceed with volume status assessment.

Step 2: Assess Volume Status

Determine intravascular volume by clinical examination and laboratory findings:

Hypovolemic Hyponatremia

Laboratory findings: Urine sodium <20 mEq/L OR Fractional excretion of sodium <1%

Extrarenal causes: Gastrointestinal losses (vomiting, diarrhea, nasogastric drainage), hemorrhage, reduced oral intake, third-space sequestration

Renal causes: Diuretic use, nephropathies, primary adrenal insufficiency, secondary adrenal disease, cerebral salt-wasting syndrome

Treatment: Address the underlying cause, restore intravascular volume - Mild cases: Oral rehydration with sodium-containing beverages (sports drinks) if tolerated - Moderate to severe: Normal saline 0.9% intravenously, titrated to clinical response - Adjust rate based on symptomatic improvement and sodium correction

Euvolemic Hyponatremia

Diagnostic approach: Urine osmolality patterns distinguish the cause

SIADH (Syndrome of Inappropriate ADH Secretion)

Urine osmolality >100 mOsm/kg (inappropriately concentrated)
Urine sodium >40 mEq/L
Euvolemic on clinical exam
Serum osmolality low despite concentrated urine

Common causes: - Malignancy: Small-cell lung cancer, pancreatic cancer, gastric cancer, genitourinary cancers, lymphomas - Pulmonary disorders: Pneumonia, tuberculosis, chronic obstructive pulmonary disease - Intracranial pathology: Head trauma, subarachnoid hemorrhage, ischemic stroke, seizures - Medications: Antipsychotics, selective serotonin reuptake inhibitors, chemotherapy agents, NSAIDs

Treatment: Free water restriction to <1000 mL daily; address underlying cause; consider vaptans for severe cases

Psychogenic Polydipsia

Urine osmolality <100 mOsm/kg (dilute)
Typically requires daily fluid intake >12 liters
Often associated with psychiatric disease
Treatment: Patient education, fluid restriction, psychiatric support

Low Solute Intake

Dilute urine (osmolality <100)
Low urine sodium (<20 mEq/L)
History of unusual diet patterns
Examples: "Tea and toast" diet in elderly, beer potomania (excessive beer consumption with minimal food)
Treatment: Nutritional counseling, increase sodium and protein intake

Hypervolemic Hyponatremia

Laboratory findings: Edema present clinically; urine sodium varies by cause

CHF (Congestive Heart Failure)

Urine sodium <10 mEq/L
Fractional excretion of sodium <1%
Mechanism: Decreased cardiac output stimulates renin-angiotensin-aldosterone system and ADH secretion
Pathophysiology: Renal arterial hypotension and hepatic congestion perpetuate sodium retention

Cirrhosis

Severe hepatic dysfunction with portal hypertension
Splanchnic arterial vasodilation leads to systemic hypotension perception
Compensatory activation of RAAS and ADH
Often associated with ascites

Nephrotic Syndrome

Severe hypoalbuminemia from proteinuria
Oncotic pressure reduction allows fluid translocation to interstitium
Compensatory RAAS and ADH activation
Sodium retention and volume expansion despite clinical appearance of depletion

Advanced Renal Failure

Urine sodium >20 mEq/L
Fractional excretion of sodium >1%
Severely reduced glomerular filtration rate impairs water and sodium excretion

Treatment: Loop diuretics (furosemide), fluid restriction, sodium restriction; address underlying cardiac or hepatic disease

Severity Classification

Severity	Sodium Level	Clinical Features
Mild	130-134 mEq/L	Often asymptomatic
Moderate	120-129 mEq/L	Nausea, headache, confusion
Severe	<120 mEq/L	Seizures, coma, cerebral edema, death

Acuity: Distinguishing Acute vs. Chronic

Acute onset (<48 hours): Brain has not had time to adapt; lower osmolar threshold before symptoms develop
Chronic onset (>48 hours): Cerebral adaptation through loss of intracellular osmolytes protects against cerebral edema

Clinical significance: Chronic hyponatremia tolerance allows lower sodium levels before symptoms; acute hyponatremia at higher levels (125-130) can cause severe neurologic symptoms

Treatment Strategy

General Principles

Identify and treat the underlying etiology
Discontinue contributory medications (SSRIs, antipsychotics, NSAIDs, diuretics)
Restrict free water intake appropriately for the volume status
Monitor closely during correction to avoid overcorrection

Specific Approaches by Volume Status

Hypovolemic: - Mild cases: Sodium-containing beverages if tolerated - Moderate/severe: Normal saline 0.9% intravenously

Euvolemic: - SIADH: Free water restriction <1000 mL daily - Low solute: Nutritional counseling, increase sodium/protein intake

Hypervolemic: - Fluid restriction (goal <1000 mL daily) - Loop diuretics (furosemide) at high doses for volume reduction

Severe/Acute Hyponatremia (Na <110 mEq/L or symptomatic with seizure/coma)

Hyponatremic Crisis Management

Administer 3% hypertonic saline 100 mL intravenous bolus
May repeat bolus up to two additional times if seizures persist
Goal is to raise sodium rapidly enough to stop cerebral edema and seizure activity
Then transition to slower correction

Correction Rate and ODS Prevention

Risk of Osmotic Demyelination Syndrome

Overly rapid sodium correction causes osmotic demyelination syndrome (ODS), characterized by myelinolysis in the pons and extrapontine regions, leading to permanent neurologic disability.

Correction limits: - Never exceed 1 mEq/L per hour - Goal: 0.25-0.5 mEq/L per hour - Maximum daily correction: 6-8 mEq/L in first 24 hours (conservative approach unless acute symptomatic) - Unless severe/acute crisis: Correct 4-6 mEq/L in <6 hours total

High-risk patients for ODS: - Severe hyponatremia (Na <105) - Concurrent hypokalemia - Alcoholic liver disease - Malnutrition - Advanced liver disease

Preventing Overcorrection

Monitor serum sodium every 1 hour during moderate/severe cases
After initial stabilization, check every 2-6 hours
Consider administering desmopressin 2 mcg intravenously every 6-8 hours to limit aquaresis if at risk for overcorrection
Prevents continued free water loss from osmotic diuresis

Intravenous Fluid Sodium Content

When choosing intravenous fluids, consider the sodium concentration:

Fluid Type	Sodium Content (mEq/L)	Use
Lactated Ringer (LR)	130	Maintenance, mild hyponatremia
Normal Saline (NS, 0.9%)	154	Hypovolemic hyponatremia
3% Hypertonic Saline	513	Severe/symptomatic hyponatremia
1/2 NS (0.45%)	77	Caution in hyponatremia; provides free water

Fluid Selection Pearls

Do not use D5W (dextrose 5% in water) in isolation for hyponatremia; high glucose becomes osmotically active
Do not use D5 1/2NS as it provides free water and worsens hyponatremia
LR and NS may actually increase serum sodium concentration if patient is significantly volume depleted, but their sodium concentrations are lower than serum so they provide relative free water at higher concentrations
Consider the underlying cause when selecting fluid (CHF needs fluid restriction, not more saline)

Hypernatremia (Serum Sodium >145 mEq/L)

Hypernatremia represents a water deficit relative to sodium stores. The pathophysiology centers on insufficient free water intake, excessive free water loss, or sodium overload. Always think of this as a water problem, not a sodium problem.

Etiology and Urine Osmolality Classification

Measure urine osmolality to determine if the kidneys are responding appropriately to hypernatremia:

Extrarenal (Renal Appropriately Concentrating)

Urine osmolality >700-800 mOsm/kg

The kidneys are concentrating urine maximally in response to hypernatremia, indicating appropriate ADH function.

Gastrointestinal losses: Diarrhea, small bowel fistulas, ileostomy
Insensible losses: Fever, sweating from exercise, mechanical ventilation, burns

Renal (Kidneys Cannot Concentrate Adequately)

Urine osmolality <700-800 mOsm/kg

The kidneys fail to concentrate urine despite hypernatremia, indicating ADH insufficiency or nephrogenic resistance.

Osmotic diuresis: Hyperglycemia, mannitol administration, contrast exposure
Loop diuretic therapy: Furosemide, torsemide
Diabetes insipidus (Central): Hypothalamic/pituitary dysfunction from trauma, surgery, granulomatous disease, malignancy
Diabetes insipidus (Nephrogenic): Kidney resistance to ADH from lithium, demeclocycline, hypercalcemia, hypokalemia

Other Mechanisms

Sodium overload: Normal saline administration, hypertonic saline, sodium bicarbonate
Impaired thirst mechanism: Elderly, altered mental status, unable to access water
Seizures or extreme exertion

Initial Workup

Check urine osmolality to guide diagnostic approach
Assess urine sodium
Evaluate volume status clinically (may be masked by hyperosmolality)
Review medications and recent procedures

Treatment Approach

The goal is slow free water replacement to avoid cerebral edema from osmotic water influx into the brain.

Step 1: Volume Resuscitation

Begin by addressing severe volume depletion if present. Be cautious: normal saline (Na 154) and lactated Ringer (Na 130) may paradoxically increase serum sodium if the patient is very hypernatremic, because their sodium concentration is less than the patient's serum sodium.

Step 2: Calculate Free Water Deficit

Use available calculators (MDCalc) to estimate total body water deficit. Formula:

Free Water Deficit (L) = Current TBW × [(Serum Na - 145) / 145]

Where total body weight = weight (kg) × age-adjusted water fraction (0.5 for older women, 0.6 for older men, 0.7 for younger men)

Step 3: Replace Free Water Deficit

Choose replacement fluid based on severity and acuity:

Fluid Choice	Sodium (mEq/L)	Use Case
Oral water	0	If safe to drink and GI intact
Nasogastric free water flush	0	If unable to drink but NG tube present
D5W (dextrose 5% water)	0 (becomes free water after glucose metabolism)	IV if necessary
1/2 NS (0.45% saline)	77	Slower correction in stable patients

Fluids to Avoid

Do NOT use normal saline (0.9%) in hypernatremia unless severe volume depletion requiring aggressive resuscitation
Do NOT use 3% saline unless there is concurrent hyponatremia or life-threatening hypernatremia
Do NOT use full NS or more concentrated solutions for deficit replacement

Step 4: Monitor and Adjust

Check serum sodium and basic metabolic panel every 4 hours initially
Transition to twice-daily monitoring once stable
Goal correction rate: 2 mEq/L per 4-hour assessment interval
Never exceed 0.5 mEq/L per hour to avoid cerebral edema
Adjust infusion rate based on response

Specific Treatment Considerations

For Osmotic Diuresis: Treat the underlying hyperglycemia or discontinue osmotic agents; this will reduce urine output and allow serum sodium to normalize more slowly

For Central Diabetes Insipidus: Replace free water deficit; may add desmopressin (synthetic ADH) if unable to replace orally

For Nephrogenic Diabetes Insipidus: Free water replacement is the mainstay; consider thiazide diuretics (which paradoxically reduce urine output in nephrogenic DI), NSAIDs, and adequate hydration

Hypokalemia (Serum Potassium <3.5 mEq/L)

Hypokalemia indicates total body potassium depletion or shift of potassium intracellularly. Even modest decreases can cause significant cardiac and muscle dysfunction.

Etiologies

Classify by mechanism and measure urine potassium (UK) and transtubular potassium gradient (TTKG) to guide diagnosis:

Transcellular Shift (UK <25 mEq/L, TTKG <3)

Potassium moves into cells; serum depletion without total body deficit

Metabolic alkalemia: Stimulates cellular uptake
Insulin administration: Drives potassium intracellularly
Catecholamine excess: Beta-2 agonists, high-dose epinephrine
Hypothermia: Shifts potassium intracellularly
Antipsychotic overdose: Clozapine causes hypokalemia through unclear mechanism

Gastrointestinal Losses (UK <25 mEq/L, TTKG <3)

Total body potassium depleted through GI tract without renal compensation

Diarrhea: Most common cause of hypokalemia
Laxative abuse
Vomiting and nasogastric suction: Indirect effect through acid loss and metabolic alkalosis
Small bowel or pancreatic fistulas

Renal Losses (UK >30 mEq/L, TTKG >7)

Kidneys unable to retain potassium despite low serum levels

Normal-to-Low Blood Pressure + Acidosis: - Diabetic ketoacidosis (despite total body depletion, serum K appears normal initially) - Renal tubular acidosis (Types 1 and 2) - Chronic diuretic use - Hypomagnesemia (most common cause of refractory hypokalemia) - Bartter syndrome (inherited; mimics chronic diuretic effect) - Gitelman syndrome (inherited; similar to Bartter but milder)

Hypertension + Hypokalemia (Mineralocorticoid Excess): - Primary hyperaldosteronism (Conn syndrome): Adrenal adenoma or bilateral hyperplasia - Secondary hyperaldosteronism: Renal artery stenosis, malignant hypertension, diuretic use - Cushing syndrome: Excessive glucocorticoid effect on mineralocorticoid receptors - Liddle syndrome: Gain-of-function mutation in renal sodium channel - Licorice ingestion: Mineralocorticoid-like effect

Clinical Manifestations

Severity	Symptoms	ECG Changes
Mild (3.0-3.5)	Often asymptomatic or vague	Minimal or absent
Moderate (2.5-3.0)	Muscle weakness, cramps, fatigue	Flattened T waves, prolonged QT
Severe (<2.5)	Paralysis, rhabdomyolysis, respiratory weakness	Prominent U waves, flattened T waves, prolonged PR interval

Serious Complications

Severe hypokalemia can cause: - Ventricular fibrillation and sudden cardiac death - Myoglobinuria and acute kidney injury from rhabdomyolysis - Respiratory muscle paralysis - Cardiac arrhythmias, especially in patients on digoxin

Diagnostic Workup

Spot urine potassium (UK) and urine sodium (UNa)
Serum magnesium level (check in all cases)
Basic metabolic panel (assess acid-base status)
12-lead ECG if K <2.6 or Mg <1.6
Transtubular potassium gradient (TTKG) = (UK × Serum osmolality) / (Serum K × Urine osmolality)
If renal losses: Blood pressure, plasma renin, aldosterone

Treatment

Always Treat Concurrent Hypomagnesemia

Magnesium depletion perpetuates hypokalemia and prevents successful potassium repletion. If serum magnesium <1.6 mEq/L, repleted concurrently using magnesium replacement protocol above.

Replacement Using Established Protocol

Follow the potassium replacement table presented in the Electrolyte Replacement Protocols section above.

Monitoring

Check serum potassium 2 hours after completing oral replacement
Recheck 2-4 hours after intravenous replacement
Place on continuous cardiac monitoring if K <2.6 or Mg <1.6

Potassium Replacement Pearls

Potassium chloride is the preferred formulation (other salts like phosphate or bicarbonate may cause other electrolyte abnormalities)
Oral potassium causes GI upset; take with food or use extended-release formulations
Expect 10 mEq replacement to raise serum K by 0.1 mEq/L (accounting for ongoing losses)
Magnesium must be repleted to prevent recurrence

Hyperkalemia (Serum Potassium >5.5 mEq/L)

Hyperkalemia represents one of the most dangerous electrolyte disturbances, capable of causing sudden cardiac death. Severe cases require immediate recognition and rapid treatment.

Etiologies

Pseudohyperkalemia (In Vitro Artifact)

Elevated potassium is a laboratory finding without true systemic hyperkalemia:

Hemolysis: Red blood cell rupture during blood draw or processing
Thrombocytosis: Potassium release from platelets during clotting (>700,000/μL)
Leukocytosis: Potassium release from white blood cells during clotting (>100,000/μL)
IV fluid contamination: Potassium-containing solution mixed into sample
Post-splenectomy: Elevated platelet counts from lack of splenic destruction

Distinction: Check plasma potassium (heparin tube) vs serum (clot tube); in pseudohyperkalemia, plasma K is normal

Transcellular Shift (Movement Into Cells)

Total body potassium normal but serum levels elevated:

Acidemia: H+ shifts into cells in exchange for K+ moving out
Insulin deficiency: DKA or severe hyperglycemia
Beta-blocker administration: Prevents normal cellular uptake
Digoxin toxicity: Inhibits Na-K-ATPase pump
Massive cellular release: Tumor lysis syndrome, rhabdomyolysis, hemolysis, crushing injuries

Renal Retention (Most Common True Hyperkalemia)

Kidneys unable to excrete potassium:

Acute kidney injury
Chronic kidney disease (especially stages 4-5)
Primary adrenal insufficiency
Medications:
ACE inhibitors (block aldosterone)
Angiotensin receptor blockers (block aldosterone)
NSAIDs (reduce renal perfusion, impair aldosterone synthesis)
Trimethoprim-sulfamethoxazole (blocks renal potassium secretion)
Heparin (suppresses aldosterone)
Potassium-sparing diuretics (spironolactone, amiloride)

Other Causes

Increased dietary potassium in susceptible patients
Potassium supplement overuse
Salt substitutes containing potassium

Clinical Manifestations

Hyperkalemia can present with nonspecific symptoms or appear asymptomatic until sudden cardiac death occurs.

Level	Symptoms	ECG Changes
5.5-6.0	Often asymptomatic	Peaked T waves (in precordial leads)
6.0-7.0	Weakness, paresthesias, palpitations	Peaked T waves, prolonged PR, widened QRS
>7.0	Severe weakness, cardiac palpitations, respiratory distress	Peaked T waves, prolonged PR, widened QRS, merged S and T (sine wave pattern)

ECG Progression and Cardiac Risk

ECG changes progress as potassium rises: 1. Peaked T waves: Most sensitive early sign 2. Prolonged PR interval: Conduction slowing 3. Widened QRS complex: Ventricular conduction delay 4. Merged S and T waves: "Sine wave" pattern indicating severe hyperkalemia 5. Eventual asystole or ventricular fibrillation: Terminal rhythm

Critical action: When ECG changes present, treat immediately regardless of exact serum level

Diagnostic Approach

Check ECG First

Before anything else: Obtain a 12-lead ECG to identify cardiac toxicity. Do not wait for confirmation; treat based on ECG findings if present.

After ECG:

Serum potassium (repeat to confirm, rule out pseudohyperkalemia)
Plasma potassium if pseudohyperkalemia suspected (heparin tube)
Basic metabolic panel (assess renal function, glucose, acid-base status)
Urine potassium, urine sodium, urine osmolality (assess renal excretion capacity)
Venous blood gas (assess for acidemia)
Complete blood count (evaluate for thrombocytosis or leukocytosis)

Treatment

Treatment intensity depends on severity, ECG findings, and renal function.

Immediate Therapy (For ECG Changes or K >7)

Agent	Dose	Onset	Mechanism	Duration
Calcium Gluconate	1-2 amps IV	<3 minutes	Stabilizes cardiac membrane	30-60 min
Insulin + Dextrose	10 U regular insulin IV + 1-2 amps D50	15-30 min	Shifts K intracellularly	4-6 hours
Albuterol	10-20 mg nebulized	15-30 min	Beta-2 agonism shifts K intracellularly	4-6 hours
Sodium Bicarbonate	1-2 amps IV	15-30 min	Shifts K intracellularly (if acidotic)	4-6 hours

Calcium Administration

Give if K >7 or ANY ECG changes present (peaked T waves or beyond)
Does not lower serum potassium; merely stabilizes cardiac membrane to prevent arrhythmia
Can repeat after 5 minutes if ECG changes persist
Onset is fastest of all hyperkalemia treatments

Shift Agents (Lower Serum Potassium 0.5-1.2 mEq/L)

Insulin + Dextrose: Most effective - Give 10 units regular insulin intravenously - Accompany with 1-2 ampules of dextrose 50% to prevent hypoglycemia - Recheck potassium in 15-30 minutes - Effect lasts 4-6 hours; may repeat if needed

Albuterol: Adjunctive therapy - 10-20 mg via nebulizer - Can combine with insulin for additive effect - Less effective in patients on chronic beta-blockers

Sodium Bicarbonate: If acidotic - 1-2 ampules IV push - Works synergistically with insulin - Essential in metabolic acidemia

Elimination Agents (Excrete Potassium from Body)

These agents remove potassium and provide definitive treatment.

Kayexalate (sodium polystyrene sulfonate): Cation exchange resin - Dose: 30-90 g orally or rectally - Onset: Several hours - Binds potassium in GI tract and removes in stool - May mix with sorbitol to promote bowel movement - Effect lasts days to weeks

Patiromer: Newer cation exchanger - Dose: 8.4-25.2 g orally daily - Onset: ~30 minutes - Well-tolerated; less GI distress than kayexalate - Particularly useful for chronic hyperkalemia management

Loop Diuretics (if not in acute kidney injury): - Furosemide ≥40 mg IV - Increases urine potassium excretion - Onset: 30 minutes - Most effective in patients with preserved renal function

Hemodialysis: For severe, refractory hyperkalemia - Most effective in setting of acute kidney injury or dialysis-requiring renal failure - Removes potassium directly - Reserved for life-threatening cases or when other measures fail

Hyperkalemia Treatment Approach

Stabilize the heart with calcium (if ECG changes present)
Shift potassium intracellularly with insulin/dextrose, albuterol, bicarbonate
Eliminate potassium from body with kayexalate, patiromer, furosemide, or dialysis
Address the underlying cause: Reduce potassium intake, discontinue ACE-I/ARB, treat acidemia
Recheck potassium: Every 2-4 hours initially until stable

Hypocalcemia (Total Calcium <8.4 mg/dL or Ionized Calcium <1.10 mmol/L)

Hypocalcemia causes neuromuscular hyperexcitability and can progress to life-threatening cardiac arrhythmias and seizures.

Etiologies

Hypoalbuminemia (Ionized Calcium Usually Normal)

Reduced albumin carries most circulating calcium; total calcium falls but ionized fraction (physiologically active) remains normal. Correct total calcium before assuming true hypocalcemia.

Hypoparathyroidism

Inadequate parathyroid hormone production: - Autoimmune destruction - Surgical removal during thyroid/parathyroid surgery - DiGeorge syndrome (22q11 deletion)

Pseudohypoparathyroidism

End-organ resistance to PTH despite elevated PTH levels

Vitamin D Deficiency

Insufficient 25(OH)D decreases intestinal calcium absorption: - Dietary insufficiency - Limited sun exposure - Malabsorption (Crohn's disease, celiac disease) - Nephrotic syndrome (loss of vitamin D binding protein)

Chronic Kidney Disease and Renal Failure

Decreased 1,25(OH)2D synthesis
Phosphate retention and hyperphosphatemia
Secondary hyperparathyroidism development

Acute Phosphate Elevation (Calcium Sequestration)

Acute pancreatitis: Saponification of fat with calcium precipitation
Tumor lysis syndrome: Massive phosphate release from dying cells
Phosphate infusion or phosphate-containing enemas

Hungry Bone Syndrome

Post-parathyroidectomy calcium influx into skeleton as parathyroid effect abruptly ceases

Clinical Manifestations

Severity	Symptoms	Signs
Mild	Perioral numbness, paresthesias	Subtle
Moderate	Muscle cramps, tetany, anxiety	Trousseau sign, Chvostek sign
Severe	Seizures, laryngospasm, cardiac arrhythmia	Loss of consciousness, airway compromise

Clinical Signs

Trousseau sign: Carpopedal spasm with blood pressure cuff inflation
Chvostek sign: Facial muscle contraction with facial nerve percussion (less specific)
Tetany: Involuntary muscle contractions
Osteomalacia: Bone pain and muscle weakness from chronic vitamin D deficiency

Diagnostic Workup

Total serum calcium and ionized calcium (if total <8.5)
Serum albumin (correct total calcium for albumin; corrected Ca = measured + 0.8 × [4.0 − albumin])
Comprehensive metabolic panel: Creatinine, phosphate, magnesium
PTH level (elevated in secondary hyperparathyroidism; low in hypoparathyroidism)
Vitamin D metabolites: 25(OH)D (storage form) and 1,25(OH)2D (active form)
12-lead ECG: Assess for QT prolongation
Consider magnesium level: Hypomagnesemia impairs PTH response

Treatment

Correct Serum Calcium for Albumin

Corrected Calcium = Measured Calcium (mg/dL) + 0.8 × (4.0 − Serum Albumin [g/dL])

This step is essential before deciding on aggressiveness of replacement.

Mild Hypocalcemia (Corrected Calcium 7.5-8.4 mg/dL)

Oral supplementation: - Calcium carbonate 1-2 g daily (taken with meals for absorption) - Calcium citrate 1-2 g daily (absorbed independently of acid) - Combined with vitamin D2 (ergocalciferol) 1000-2000 IU daily or vitamin D3 (cholecalciferol) 1000-2000 IU daily

Treatment duration: Days to weeks; recheck serum calcium weekly

Severe Hypocalcemia (Corrected Calcium <7.5 mg/dL or Symptomatic)

Intravenous calcium gluconate (preferred over calcium chloride outside central lines): - Dose: 1-2 grams intravenously over 20 minutes - Prepare as: 10 mL of 10% solution (1 gram) per 50-100 mL normal saline - Can repeat infusion if symptoms persist or calcium remains critically low - Recheck serum calcium 2 hours after infusion

IV Calcium Administration

Do NOT mix with phosphate (forms precipitate)
Do NOT infuse rapidly (causes cardiac arrhythmias, hypotension)
Consider central line if repeated infusions anticipated (calcium gluconate is caustic to peripheral veins)
Dilute appropriately in normal saline
Monitor ECG during administration

Magnesium Repletion

Always check and correct hypomagnesemia if present (serum Mg <1.6 mEq/L) using magnesium replacement protocol above. Hypomagnesemia impairs the PTH response and perpetuates hypocalcemia.

Address Underlying Cause

Vitamin D deficiency: Vitamin D supplementation (dose depends on 25[OH]D level and renal function)
Hypoparathyroidism: Calcium and vitamin D replacement
Acute kidney injury: Phosphate binders, treat hyperphosphatemia
Pancreatitis: Supportive care; usually self-limited
Tumor lysis: Aggressive hydration, allopurinol or febuxostat

Hypercalcemia (Serum Calcium >10.5-11 mg/dL; Severe Crisis: 14-16 mg/dL)

Hypercalcemia is a medical emergency when severe, as it causes dehydration, nephrogenic diabetes insipidus, cardiac arrhythmias, and altered mental status.

Etiologies

Only two diagnoses account for >90% of hypercalcemia cases: primary hyperparathyroidism and malignancy.

Primary Hyperparathyroidism

PTH-secreting parathyroid adenoma, hyperplasia, or rarely carcinoma. Accounts for approximately 50% of hypercalcemia in ambulatory settings.

PTHrP secretion (squamous cell lung cancer, renal cell carcinoma, breast cancer, ovarian cancer): Most common mechanism in hospitalized patients
Osteolytic metastases: Direct bone destruction (breast cancer, lymphoma)
Calcitriol production by tumor: Lymphomas (Hodgkin and non-Hodgkin), tuberculosis, histoplasmosis

Vitamin D Excess

Exogenous supplementation: Toxic megadoses
Endogenous overproduction: Granulomatous diseases (sarcoidosis, tuberculosis, fungal infections), lymphomas

Increased Bone Turnover

Hyperthyroidism
Thyrotoxicosis
Immobilization (especially in young, active individuals)
Vitamin A toxicity
Paget disease (if immobilized)

Medications

Thiazide diuretics: Decrease urinary calcium excretion
Lithium: Raises PTH set point
Vitamin D intoxication: From supplements or granulomatous disease

Milk-Alkali Syndrome

Excessive calcium and alkali (calcium carbonate + sodium bicarbonate) causing hypercalcemia, metabolic alkalosis, and renal insufficiency

Clinical Manifestations

"Stones, bones, groans, and psychiatric overtones"

System	Manifestations
Renal	Nephrogenic DI (polyuria, polydipsia), acute kidney injury, kidney stones
GI	Nausea, vomiting, constipation, anorexia, peptic ulcer disease
Neuro	Altered mental status, confusion, lethargy, coma, headache
Cardiac	Arrhythmias, hypertension, shortened QT interval
Musculoskeletal	Bone pain, osteoporosis with fractures
Metabolic	Dehydration, metabolic alkalosis

Diagnostic Workup

PTH: The Most Important Initial Test

Always obtain serum PTH level early. This single test narrows the differential dramatically.

Serum PTH (most important initial test)
Ionized calcium (if total calcium abnormal)
Basic metabolic panel: Assess creatinine, phosphate
Complete blood count: Evaluate for lymphoma
Chest X-ray: Evaluate for sarcoidosis or malignancy
12-lead ECG: Assess for shortened QT interval
Vitamin D metabolites: 25(OH)D and 1,25(OH)2D if PTH suppressed
PTHrP level if PTH low and malignancy suspected

Interpretation Framework

If PTH elevated (>65 pg/mL): - Primary hyperparathyroidism (most common) - Check 24-hour urine calcium to distinguish from familial hypocalciuric hypercalcemia (FHH) - FHH: Very low urinary calcium (<100 mg/24h) - Primary hyperparathyroidism: Normal to high urinary calcium

If PTH suppressed (low): - Measure PTHrP (PTH-related peptide) - If elevated: Malignancy with PTHrP secretion - Measure vitamin D metabolites - If 1,25(OH)2D elevated: Granulomatous disease or lymphoma producing calcitriol - If 25(OH)D elevated: Exogenous vitamin D toxicity - Evaluate for osteolytic metastases, vitamin A toxicity, thiazide use

Treatment Strategy

Treatment intensity correlates with severity and symptoms. Asymptomatic mild hypercalcemia may be monitored; severe symptomatic hypercalcemia requires aggressive management.

Mild Hypercalcemia (Corrected Calcium <12 mg/dL, Asymptomatic)

Conservative approach: - Avoid thiazide diuretics (worsen hypercalcemia) - Avoid lithium (raises PTH set point) - Restrict dietary calcium intake - Ensure adequate hydration - Address underlying cause (parathyroidectomy for primary hyperparathyroidism) - Monitor serum calcium every 3-6 months

Moderate Hypercalcemia (Calcium 12-14 mg/dL)

Aggressive hydration + pharmacologic treatment:

Intervention	Dose/Details	Onset
IV Normal Saline	200-300 mL/hour	Immediate
Furosemide	20-40 mg IV every 4-6 hours (after volume repletion)	30-60 min
Calcitonin	4 U/kg IV or IM every 12 hours	2-4 hours
Bisphosphonate	Zoledronic acid 4 mg IV over 15 minutes (or pamidronate 60-90 mg)	3-5 days

Mechanism: - IV saline: Restores intravascular volume, promotes renal calcium wasting - Furosemide: Loop diuretic prevents excessive fluid expansion; promotes calcium excretion - Calcitonin: Inhibits osteoclast-mediated bone resorption; rapid onset but tachyphylaxis develops - Bisphosphonate: Blocks osteoclast bone resorption; slower onset but longer duration

Severe Hypercalcemia (Calcium >14 mg/dL or Life-Threatening Symptoms)

All measures above plus:

Treatment	Details
Aggressive IV hydration	Fluid challenge; place central line if needed
Calcitonin	As above; addresses acute crisis
Bisphosphonate	As above
Hemodialysis	Consider if:Renal failure present; Unable to tolerate large fluid volumes (CHF, renal disease)
Glucocorticoids	40-60 mg prednisone daily if granulomatous disease or lymphoma (calcitriol overproduction)
Ketoconazole	For granulomatous disease with excessive calcitriol production (coccidioidomycosis, histoplasmosis)

Severe Hypercalcemia Management

In life-threatening hypercalcemia: - Start IV saline immediately (rates of 300-500 mL/hour) - Add calcitonin and bisphosphonate simultaneously - Monitor urine output, serum calcium, renal function closely - Have hemodialysis capability available if renal failure present - Treat underlying malignancy or parathyroid disease

Acid-Base Disorders

Acid-base interpretation requires systematic evaluation of arterial (or venous) blood gas with clinical context. A structured approach prevents errors and guides appropriate treatment.

Normal Values and Basic Concepts

Parameter	Normal Range	Interpretation
pH	7.35-7.45	Acidemia <7.35; Alkalemia >7.45
pCO2	35-45 mmHg	Reflects respiratory component
HCO3-	22-26 mEq/L	Reflects metabolic component

Arterial vs Venous Blood Gas

ABG (Arterial): More accurate for pCO2; gold standard for acid-base assessment
VBG (Venous): Acceptable surrogate in many clinical settings
Concordant values: pH (add ~0.04 to VBG pH to approximate ABG), HCO3-
Non-concordant: pCO2 differs between ABG and VBG; ABG required if pCO2 critical

Systematic Interpretation Approach

Step-by-Step Interpretation

Step 1: Identify Acidemia or Alkalemia

Determine if pH is low (<7.35) or high (>7.45).

Step 2: Identify Primary Process

Look at the respiratory and metabolic components: - Metabolic acidosis: Low HCO3- with low pH - Metabolic alkalosis: High HCO3- with high pH - Respiratory acidosis: High pCO2 with low pH - Respiratory alkalosis: Low pCO2 with high pH

The parameter that matches the pH direction is the primary disorder.

Step 3: Check Respiratory Compensation

Determine if respiratory response is appropriate for the primary process.

For Metabolic Acidosis — Use Winter's Formula:

Expected pCO2 = (HCO3- × 1.5) + 8 ± 2

Actual pCO2 > Expected: Concurrent respiratory acidosis
Actual pCO2 < Expected: Concurrent respiratory alkalosis
Actual pCO2 ≈ Expected: Appropriate respiratory response

For Metabolic Alkalosis — Expected pCO2 rises 6-7 mmHg per 10 mEq/L rise in HCO3-:

If actual pCO2 lower than expected: Concurrent respiratory alkalosis
If actual pCO2 higher than expected: Concurrent respiratory acidosis

For Respiratory Acidosis:

Duration	Expected HCO3- Change Per 10 mmHg pCO2 Rise
Acute (<24 hours)	+1 mEq/L
Chronic (>24-48 hours)	+3-4 mEq/L

For Respiratory Alkalosis:

Duration	Expected HCO3- Change Per 10 mmHg pCO2 Drop
Acute (<24 hours)	-2 mEq/L
Chronic (>24-48 hours)	-4-5 mEq/L

Step 4: Calculate Anion Gap (for Metabolic Acidosis)

Anion Gap = [Na+] − ([Cl−] + [HCO3−])

Normal anion gap = 12 ± 2 mEq/L (can vary by laboratory)

Elevated anion gap = >14 mEq/L

Step 5: Delta-Delta (for Anion Gap Metabolic Acidosis)

When anion gap metabolic acidosis is identified, calculate whether a concurrent non-anion gap metabolic acidosis or metabolic alkalosis exists.

ΔAG = Change in Anion Gap = Measured AG − 12 ΔHCO3- = Change in HCO3- = 24 − Measured HCO3- ΔΔ = ΔAG / ΔHCO3-

Interpretation: - ΔΔ <1: Concurrent non-AG metabolic acidosis (HCO3- dropping faster than AG rising) - ΔΔ 1-2: Pure AG metabolic acidosis (appropriate relationship) - ΔΔ >2: Concurrent metabolic alkalosis (HCO3- not dropping as much as AG rising)

Metabolic Acidosis

Metabolic acidosis results from either bicarbonate loss or hydrogen ion accumulation.

Anion Gap vs. Non-Anion Gap Classification

Anion Gap Metabolic Acidosis (AG >14)

The anion gap exists because unmeasured anions accumulate to balance sodium. Common mnemonic: MUDPILES

Cause	Mechanism	Notes
Methanol	Toxic metabolite formic acid	Osmolar gap present; visual symptoms
Uremia	Retention of organic acids	Late in renal failure; AG usually <20
DKA	Ketone accumulation	Glucose >250; check beta-hydroxybutyrate
Propylene glycol	Toxic metabolite	Often iatrogenic (medications, IV solutions)
Isoniazid	Toxic metabolite	Tuberculosis treatment
Lactic acidosis	Lactate accumulation	Type A (hypoxemia) or Type B (mitochondrial)
Ethylene glycol	Toxic metabolite oxalic acid	Antifreeze ingestion; calciums oxalate crystals in urine
Salicylates	Aspirin toxicity	Mixed respiratory alkalosis + metabolic acidosis

Winter's Formula Interpretation

Always calculate expected pCO2 using Winter's formula for any AG metabolic acidosis: - If actual pCO2 > expected → Concurrent respiratory acidosis - If actual pCO2 < expected → Concurrent respiratory alkalosis (typical in early DKA, lactic acidosis, and salicylate toxicity)

Non-Anion Gap Metabolic Acidosis

The anion gap is normal, but HCO3- is low. Causes involve GI bicarbonate loss or renal hydrogen ion retention. Determine using Urine Anion Gap (UAG).

UAG = [UNa+] + [UK+] − [UCl−]

Urine Anion Gap	Interpretation	Common Causes
UAG Positive (>0)	Kidney cannot acidify urine; distal acidification defect	RTA Type 1, RTA Type 4, Chronic kidney disease
UAG Negative (<-20)	Appropriate acid excretion; GI bicarbonate loss	Diarrhea (most common), small bowel fistulas, ileostomy

Treatment

Identify and treat the underlying cause (remove toxin, treat infection, control diabetes)
In severe acidemia (pH <7.1), consider sodium bicarbonate 100-150 mEq IV over 1-2 hours for metabolic acidosis, especially if severe and refractory
In DKA: Insulin and fluids (bicarbonate generally avoided unless pH <6.9)
In lactic acidosis: Treat underlying shock, improve tissue perfusion

Respiratory Acidosis

Respiratory acidosis results from inadequate ventilation, causing carbon dioxide retention.

Acute vs. Chronic Distinction

The kidney's ability to retain bicarbonate determines compensation:

For every 10 mmHg rise in pCO2 above 40: - Acute respiratory acidosis (<24 hours): HCO3- rises by 1 mEq/L (minimal renal compensation) - Chronic respiratory acidosis (>24-48 hours): HCO3- rises by 3-4 mEq/L (metabolic compensation)

Etiologies

Category	Examples
CNS Depression	Sedatives, opioids, anesthetics, head trauma, sleep apnea
Neuromuscular Disorder	Myasthenia gravis, Guillain-Barre syndrome, polymyositis, amyotrophic lateral sclerosis
Chest Wall Abnormality	Flail chest, rib fractures, restrictive lung disease, severe obesity
Upper Airway Obstruction	Epiglottitis, foreign body, laryngospasm
Lower Airway/Lung Disease	COPD exacerbation, asthma, pneumonia, pulmonary edema, pulmonary fibrosis
Air Trapping	COPD with auto-PEEP, asthma, emphysema

Treatment

Identify and treat underlying cause
Improve ventilation: Non-invasive positive pressure (CPAP, BiPAP) or mechanical ventilation if needed
Support oxygenation
Address concurrent metabolic abnormalities

Respiratory Alkalosis

Respiratory alkalosis results from hyperventilation, causing excessive carbon dioxide elimination.

Acute vs. Chronic Distinction

For every 10 mmHg drop in pCO2 below 40: - Acute respiratory alkalosis (<24 hours): HCO3- drops by 2 mEq/L (minimal renal compensation) - Chronic respiratory alkalosis (>24-48 hours): HCO3- drops by 4-5 mEq/L (metabolic compensation through increased urinary bicarbonate wasting)

Etiologies

Cause	Mechanism
Pain	Splinting from acute pain, rib fractures, abdominal trauma
Anxiety	Panic attacks, hyperventilation syndrome
Hypoxemia	Fever, infection, pulmonary embolism, pneumonia, high altitude
Drugs	Salicylates (aspirin), stimulants, amphetamines
Fever	Increased metabolic rate drives hyperventilation
Pregnancy	Progesterone-mediated stimulation of respiratory center
Sepsis	Cytokine-mediated hyperventilation as early sign
Intracranial Pathology	Head trauma, intracerebral hemorrhage, seizures
Mechanical Ventilation	Overly aggressive ventilator settings

Treatment

Address underlying cause (treat infection, manage pain, reassure anxious patient)
For hyperventilation from anxiety: Breathing exercises, rebreather bag if severe
Adjust mechanical ventilation if iatrogenic
Avoid overcorrection (overly rapid increase in pCO2 causes metabolic acidosis paradoxically)

Metabolic Alkalosis

Metabolic alkalosis results from bicarbonate excess or hydrogen ion loss. Classification by responsiveness to saline helps guide treatment.

Saline-Responsive Alkalosis (Urine Chloride <20 mEq/L)

Kidneys will excrete bicarbonate if given normal saline, indicating volume depletion as primary driver.

Causes: - Vomiting and nasogastric suction: Direct loss of hydrogen and chloride; metabolic alkalosis - Diuretic use: Loop and thiazide diuretics cause volume depletion and trigger RAAS activation - GI losses of hydrochloric acid: Small bowel/pancreatic fistulas

Treatment: Normal saline 0.9% IV at rates sufficient to correct volume deficit; typically 250-500 mL/hour. Potassium replacement often necessary simultaneously.

Saline-Resistant Alkalosis (Urine Chloride >20 mEq/L)

Kidneys cannot excrete bicarbonate because RAAS is activated from other mechanisms. Further saline worsens alkalosis.

Hypertensive Variants (Blood Pressure Elevated)

Primary hyperaldosteronism (Conn syndrome): - Autonomous aldosterone secretion from adrenal adenoma or bilateral hyperplasia - Severe hypokalemia - Low plasma renin - Elevated plasma aldosterone - Treatment: Spironolactone (aldosterone antagonist) or amiloride (potassium-sparing diuretic)

Secondary hyperaldosteronism from hypertension: - Renal artery stenosis, malignant hypertension, uncontrolled hypertension - RAAS activation from perceived hypoperfusion - Treatment: Control blood pressure; add potassium-sparing diuretics or ACE inhibitors

Cushing syndrome: Excess glucocorticoid effects on mineralocorticoid receptors - Treatment: Treat underlying pituitary or adrenal disease

Normotensive Variants (Blood Pressure Normal)

Severe hypokalemia: - Hypokalemia perpetuates alkalosis through multiple mechanisms - Treatment: Potassium replacement using protocols above; may require high doses

Bartter and Gitelman syndromes: Inherited renal tubular disorders - Mimic chronic diuretic use - Severe hypokalemia and alkalosis - Treatment: NSAIDs, potassium-sparing diuretics, amiloride

Respiratory Compensation in Metabolic Alkalosis

Respiratory response is typically minimal in metabolic alkalosis (unlike metabolic acidosis where hyperventilation is prominent). The respiratory system poorly matches alkalosis because hypoxemia is less tolerable than mild hypercapnia.

Expected pCO2 elevation: Approximately 6-7 mmHg per 10 mEq/L rise in HCO3-.

Treatment Strategy

Alkalosis Type	Primary Treatment
Saline-responsive	Normal saline IV (0.9%) + potassium chloride replacement
Saline-resistant, Hypertensive	Antihypertensive agents (ACE inhibitors, ARBs); Aldosterone antagonists if appropriate
Saline-resistant, Normotensive	Potassium replacement (often high-dose); NSAIDs; Potassium-sparing diuretics
Severe (pH >7.6)	Hydrochloric acid or acetazolamide in addition to above measures

Summary: Quick Reference Table

Abnormality	Key Diagnostic Finding	Initial Treatment	Critical Monitoring
Hypokalemia	K <3.5; TTKG <3 if renal cause	Replace per protocol; always check Mg	Recheck K in 2h; ECG if K <2.6
Hyperkalemia	K >5.5; peaked T waves on ECG	Calcium (stabilize), insulin/dextrose (shift), kayexalate (eliminate)	ECG first; recheck K q2-4h
Hyponatremia	Na <135; measured osm < calculated	Identify cause; free water restriction ±saline	Correct slowly; avoid ODS; check Na q1-2h
Hypernatremia	Na >145; free water deficit	Calculate deficit; replace with free water	Correct slowly (0.25-0.5 mEq/L/hr); check Na q4h
Hypocalcemia	Ca <8.4; correct for albumin	IV calcium gluconate if severe; oral Ca + vitamin D	Recheck Ca 2h after IV; check Mg
Hypercalcemia	Ca >10.5; check PTH	IV saline + calcitonin ± bisphosphonate	Hourly Ca if >14; assess renal function
AG Metabolic Acidosis	HCO3- low; AG >14; Winter's formula	Treat underlying cause (DKA, lactic acidosis, toxins)	Follow pH, anion gap closure
Non-AG Metabolic Acidosis	HCO3- low; AG normal; UAG negative	Treat diarrhea; identify RTA type if UAG positive	Correct slowly with bicarbonate
Respiratory Acidosis	pH <7.35; pCO2 >45	Improve ventilation; identify CNS/NM/airway cause	Serial ABGs; support ventilation
Respiratory Alkalosis	pH >7.45; pCO2 <35	Treat underlying cause; avoid overcorrection	Follow pCO2 trend; prevent paradoxical acidosis
Metabolic Alkalosis	pH >7.45; HCO3- >26; UCl <20 (saline-responsive)	Normal saline + KCl; identify etiology	Check BP; correct K concurrently

Clinical Pearls and Key Take-Homes

Always Remember

Magnesium: Check in all hypokalemia and hypomagnesemia independently; repletion is essential for K correction success
Volume status: Critical for guiding hyponatremia treatment; never give hypertonic saline to euvolemic patient
ECG in hyperkalemia: Check it first, before waiting for lab confirmation; peaked T waves demand treatment
Winter's formula: Use in every case of metabolic acidosis to identify concurrent respiratory disorders
Anion gap: Calculate in all metabolic acidosis; use Delta-Delta to identify mixed disorders
Correction rates: Hyponatremia and hypernatremia both require slow correction (0.25-0.5 mEq/L per hour) to avoid osmotic demyelination
Pseudohyperkalemia: Repeat potassium in plasma (heparin tube) if hemolysis, thrombocytosis, or leukocytosis present
Albumin correction: Always correct calcium for serum albumin before determining aggressiveness of supplementation
Renal function: Tailor electrolyte replacement aggressiveness to renal function; aggressive repletion in ESRD causes harm
Underlying cause: Treating the root disorder is always more important than just correcting numbers

Last update: April 12, 2026