Topic map

1. Foundations
   • Body-water compartments, osmolality, renal and hormonal regulation
   • How to interpret an electrolyte panel, albumin, glucose, renal function, acid-base status, and ECG
2. Sodium disorders
   • Hyponatremia: hypotonic, isotonic, hypertonic; hypovolemic/euvolemic/hypervolemic forms; SIADH; emergency correction and avoiding osmotic demyelination
   • Hypernatremia: water loss versus sodium gain; safe replacement and avoiding cerebral edema
3. Potassium disorders
   • Hypokalemia: causes, ECG findings, oral/IV replacement, magnesium correction
   • Hyperkalemia: ECG risk, immediate cardiac stabilization, intracellular shifting, potassium removal, dialysis indications
4. Calcium disorders
   • Hypocalcemia: albumin correction, ionized calcium, hypoparathyroidism, vitamin D deficiency, acute IV calcium
   • Hypercalcemia: PTH-dependent versus PTH-independent causes, IV fluids, calcitonin, bisphosphonates, denosumab, dialysis
5. Magnesium disorders
   • Hypomagnesemia: arrhythmia, refractory hypokalemia/hypocalcemia, replacement
   • Hypermagnesemia: renal failure and magnesium-containing medicines, IV calcium and dialysis
6. Phosphate disorders
   • Hypophosphatemia: refeeding syndrome, respiratory weakness, replacement
   • Hyperphosphatemia: kidney disease, binders, diet, dialysis
7. Chloride and bicarbonate
   • Hyperchloremic metabolic acidosis, chloride-responsive metabolic alkalosis, saline effects, acid-base interpretation
8. Integrated clinical approach
   • Emergency red flags, fluid selection, monitoring, common errors, and worked cases.

Sodium disorders: diagnostic and treatment algorithms

1. First steps for any abnormal sodium

Immediate assessment

1. Confirm and assess urgency
   • Repeat sodium if unexpected or inconsistent with the clinical picture.
   • Assess mental status, seizure, headache, vomiting, respiratory status, urine output, volume status.
   • Obtain ECG if there are other electrolyte abnormalities or severe illness.
2. Establish timing
   • Acute: known onset in <48 hours.
   • Chronic or unknown duration: ≥48 hours or unclear. Treat as chronic for safety.
3. Check key tests
   • Serum glucose, urea/creatinine, potassium, chloride, bicarbonate.
   • Serum osmolality.
   • Urine osmolality and urine sodium, ideally before IV fluids or diuretics if doing so does not delay treatment.
   • Thyroid-stimulating hormone and morning cortisol when euvolemic hypotonic hyponatremia is unexplained.
   • Review drugs: thiazides, SSRIs/SNRIs, antipsychotics, carbamazepine/oxcarbazepine, desmopressin, NSAIDs, opioids, chemotherapy, lithium, laxatives, and diuretics.
4. Treat life-threatening symptoms before completing the workup.

Part A: Hyponatremia

Definition and clinical danger

• Mild: nausea, headache, impaired attention, gait instability.
• Moderate: vomiting, confusion, lethargy, delirium.
• Severe: seizure, obtundation, coma, respiratory arrest.

Hyponatremia algorithm 1: emergency triage

Low serum sodium
        |
        v
Seizure, coma, profound confusion, cardiorespiratory distress,
or other severe neurologic symptoms?
        |
   Yes  |  No
        | 
        v
Give 3% hypertonic saline in a monitored setting
        |
Aim for early rise of 4-6 mmol/L, enough to reverse immediate cerebral edema
        |
Check sodium frequently and stop hypertonic saline once symptoms improve
or early target reached
        |
Then identify cause and prevent overcorrection

Emergency treatment: severely symptomatic hyponatremia

• 100 mL 3% saline IV over 10 minutes, repeat up to two additional times if severe symptoms persist, checking sodium between boluses when feasible.

• Serum sodium every 2-4 hours during active correction, more frequently if brisk water diuresis or high risk of overcorrection.
• Strict input-output record and urine output.
• Neurologic status.
• Potassium, because potassium repletion itself raises serum sodium.

• ≤8 mmol/L in 24 hours in people at high risk of ODS.
• Many protocols allow ≤10 mmol/L in the first 24 hours and ≤8 mmol/L for each subsequent 24 hours in lower-risk patients, but more conservative targets are often preferred.

If sodium is correcting too fast

Sodium rise approaching/exceeding target
        |
        v
Stop hypertonic saline and other sodium-raising therapy
        |
        v
Consider desmopressin to stop water diuresis
        |
        v
Give electrolyte-free water, commonly IV D5W, to relower sodium
under specialist guidance
        |
        v
Continue frequent sodium testing

Hyponatremia algorithm 2: classify by tonicity

Hyponatremia
    |
    v
Measure serum osmolality
    |
    +--> High (>295 mOsm/kg): hypertonic hyponatremia
    |       Usually hyperglycemia, mannitol, radiocontrast or other effective osmoles
    |
    +--> Normal (about 275-295): isotonic hyponatremia
    |       Consider pseudohyponatremia from marked hyperlipidemia/proteinemia
    |
    +--> Low (<275): true hypotonic hyponatremia
            |
            v
       Measure urine osmolality
            |
            +--> <100 mOsm/kg
            |       Excess water intake / low solute intake
            |       Examples: primary polydipsia, beer potomania, “tea and toast”
            |
            +--> ≥100 mOsm/kg
                    ADH is active
                    |
                    v
                Assess volume status and urine sodium

Correct sodium for hyperglycemia

Hyponatremia algorithm 3: true hypotonic hyponatremia by volume state

A. Hypovolemic hypotonic hyponatremia

• Vomiting, diarrhea, burns, third spacing.
• Diuretics, especially thiazides.
• Mineralocorticoid deficiency.
• Cerebral salt wasting is uncommon and requires careful diagnosis.

• Orthostasis, tachycardia, dry mucosa, low JVP, reduced urine output.
• Urine Na often <30 mmol/L in extrarenal sodium loss.
• Urine Na often ≥30 mmol/L with renal salt loss, diuretics, adrenal insufficiency, or kidney disease.

Hypovolemic hypotonic hyponatremia
        |
        v
Stop cause where possible: e.g., thiazide, GI losses
        |
        v
If unstable: resuscitate with 0.9% saline
        |
        v
If stable: 0.9% saline and replace ongoing losses
        |
        v
Monitor Na closely - restoration of volume may abruptly suppress ADH,
causing rapid water diuresis and overcorrection
        |
        v
Check/replace potassium and evaluate cortisol if appropriate

B. Euvolemic hypotonic hyponatremia

• SIADH.
• Medications, particularly SSRIs, carbamazepine, oxcarbazepine, antipsychotics, opioids, and some anticancer drugs.
• Pain, nausea, pulmonary disease, central nervous system disorders.
• Hypothyroidism, usually severe.
• Glucocorticoid deficiency.
• Primary polydipsia or low solute intake.

• Low serum osmolality.
• Urine osmolality >100 mOsm/kg, often substantially higher.
• Urine sodium generally >30 mmol/L with normal salt intake.
• Clinically euvolemic.
• No adrenal insufficiency, substantial hypothyroidism, kidney failure, or recent diuretic explanation.

Euvolemic hypotonic hyponatremia
        |
        v
Exclude/treat adrenal insufficiency and clinically important hypothyroidism
Stop culprit medication if feasible
Treat pain, nausea, pulmonary/CNS trigger
        |
        v
If severe symptoms: 3% saline pathway first
        |
        v
If chronic/mild-moderate and stable:
fluid restriction, often 500-1,000 mL/day
        |
        v
Reassess Na and urine osmolality after 24-48 h
        |
        +--> Responding: continue and treat cause
        |
        +--> Not responding: specialist-directed increase in solute
             (oral urea is increasingly used), loop diuretic plus oral NaCl
             in selected cases, or carefully selected vasopressin antagonist

C. Hypervolemic hypotonic hyponatremia

• Heart failure.
• Cirrhosis.
• Nephrotic syndrome.
• Advanced kidney failure.

Hypervolemic hypotonic hyponatremia
        |
        v
Treat underlying disorder
        |
        v
Restrict fluid and sodium
        |
        v
Use loop diuretic if congestion and kidney function permit
        |
        v
Optimize heart failure/cirrhosis/renal treatment
        |
        v
Consider specialist advice for vaptan or renal replacement therapy
in selected refractory cases

Practical hyponatremia warnings

• Do not correct to normal rapidly. Correct enough to stabilize symptoms, then slow down.
• Do not give 0.9% saline reflexively to all hyponatremic patients. In SIADH, sodium may be excreted while water is retained.
• Correct potassium. Potassium depletion contributes to hyponatremia and to ODS risk. Its replacement can raise serum sodium.
• Stop thiazides in thiazide-associated hyponatremia.
• Check cortisol before accepting a diagnosis of SIADH.
• In acute water intoxication from endurance exercise, MDMA, or psychogenic polydipsia, neurologic symptoms can progress rapidly even if the sodium is not extremely low.

Part B: Hypernatremia

Definition and clinical danger

• Thirst, weakness, irritability, lethargy.
• Hyperreflexia, myoclonus, confusion.
• Seizures and coma in severe or rapidly developing cases.

Hypernatremia algorithm 1: classify volume status

Hypernatremia
      |
      v
Assess circulation/volume status
      |
      +--> Hypovolemic: water loss exceeds sodium loss
      |    Examples: diarrhea, sweating, burns, osmotic diuresis
      |
      +--> Euvolemic: predominantly pure water loss
      |    Examples: central or nephrogenic diabetes insipidus,
      |    insensible loss with no water intake
      |
      +--> Hypervolemic: sodium gain exceeds water gain
           Examples: hypertonic saline/bicarbonate, salt poisoning,
           mineralocorticoid excess

Hypernatremia algorithm 2: immediate treatment

Hypernatremia
      |
      v
Shock or severe intravascular volume depletion?
      |
 Yes  | No
      |
      v
Restore circulation first with isotonic crystalloid (0.9% saline
or balanced crystalloid as clinically appropriate)
      |
      v
Then replace free water deficit and ongoing water losses
      |
      v
Choose rate based on acuity:
- acute, documented <48 h: more rapid correction may be appropriate
- chronic/unknown: controlled correction over about 48-72 h
      |
      v
Monitor Na every 2-4 h initially and adjust

Estimate the free-water deficit

• Adult man: 0.6 × body weight in kg
• Adult woman: 0.5 × body weight in kg
• Older man: about 0.5 × weight
• Older woman: about 0.45 × weight
• Obesity: use lower fractions.

Example

• Maintenance water requirements.
• Ongoing renal, gastrointestinal, and insensible losses.
• Any required replacement of potassium or other electrolytes.

Hypernatremia algorithm 3: choose fluid and rate

A. Acute hypernatremia, clearly developed within <48 hours

• Brain cells have not fully adapted, so correction can be faster than in chronic disease.
• The exact rate is individualized, typically in an ICU or monitored setting for severe cases.
• Use enteral water when safe, or IV D5W; use 0.45% saline when both water and sodium replacement are needed.

B. Chronic or unknown-duration hypernatremia

• Lower sodium by no more than about 0.5 mmol/L/hour.
• Aim for ≤10-12 mmol/L in 24 hours.
• Replace the water deficit over approximately 48-72 hours, while reassessing repeatedly.

C. Fluid choice by clinical setting

Hypernatremia algorithm 4: use urine studies to find the cause

Hypernatremia
      |
      v
Measure urine volume and urine osmolality
      |
      +--> Polyuria + urine osmolality <300 mOsm/kg:
      |    diabetes insipidus is likely
      |       |
      |       +--> Desmopressin response: central DI likely
      |       |
      |       +--> Little/no response: nephrogenic DI likely
      |
      +--> Polyuria + higher urine osmolality:
      |    osmotic diuresis, often glucose, urea, mannitol, diuretics
      |
      +--> Low urine volume + concentrated urine:
           extrarenal water loss or inadequate water intake

Diabetes insipidus: treatment principles

• Causes include pituitary/hypothalamic disease, neurosurgery, head trauma, infiltrative disease, and idiopathic disease.
• Treat water deficit and use desmopressin when appropriate.
• Monitor closely because desmopressin plus unrestricted water intake can cause hyponatremia.

• Common cause: lithium. Also hypercalcemia, hypokalemia, kidney disease, obstruction, and certain drugs.
• Stop or reduce the cause if feasible.
• Correct hypercalcemia/hypokalemia.
• Specialist options include low-solute diet, thiazide therapy, amiloride for lithium-associated disease, and selected use of NSAIDs.

High-yield comparison

Bedside checklist

• Onset: acute, chronic, or unknown.
• Neurologic symptoms and severity.
• Volume status and hemodynamics.
• Serum osmolality and glucose.
• Urine osmolality, urine sodium, urine output.
• Medicines and recent IV-fluid exposure.
• Sodium target over the next 6 and 24 hours.
• Frequency of sodium checks.
• Explicit plan if sodium corrects too quickly or too slowly.