ELECTROLYTES

Hyponatraemia 

this link is very good : https://www.psychdb.com/cl/hyponatremia

Differentials

Pseudohyponatraemia (lab artifact)

  • Hyperlipidaemia
  • Hyperglycaemia (translocational hyponatraemia)
  • Hyperproteinaemia (e.g., multiple myeloma)

Hypervolaemic Hyponatraemia (ECF ↑)

  • Congestive cardiac failure (CCF)
  • Chronic liver disease (cirrhosis)
  • Chronic kidney disease (CKD)
  • Nephrotic syndrome
  • Hepatorenal syndrome
  • Corticosteroid use (↑ mineralocorticoid effect)

Euvolaemic Hyponatraemia (ECF normal)

  • Syndrome of Inappropriate ADH secretion (SIADH)
    • Medications: SSRIs, TCAs, carbamazepine, cyclophosphamide, vincristine, antipsychotics
    • Malignancy: small cell lung carcinoma, pancreatic, prostate, leukaemia, cervical cancers
  • Hypothyroidism
  • Secondary adrenal insufficiency
  • Water intoxication (e.g., psychogenic polydipsia)
  • “Beer potomania” (low solute intake)

Hypovolaemic Hyponatraemia (ECF ↓)

  • GI losses: diarrhoea, vomiting
  • Excessive sweating
  • Burns
  • Fistula losses
  • Villous adenoma (rectal)
  • Addison’s disease (primary adrenal insufficiency)
  • Diuretics (especially thiazides)
…………………….https://i0.wp.com/lifeinthefastlane.com/wp-content/uploads/2010/06/Hyponatraemia-Flow1.jpg?ssl=1
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Clinical Features of Hyponatraemia

Severity of symptoms is related to the rapidity and extent of sodium decline.

  • Serum Na⁺ > 125 mmol/L
    • Typically asymptomatic
  • Serum Na⁺ 115–125 mmol/L
    • Lethargy
    • Confusion
    • Anorexia
    • Nausea and vomiting
  • Serum Na⁺ < 115 mmol/L
    • Muscle cramps and weakness
    • Seizures
    • Coma

Key Clinical Considerations

  • Identify potential underlying causes
    • History of fluid losses (e.g. vomiting, diarrhoea, burns)
    • History of excessive fluid intake (e.g. psychogenic polydipsia)
    • Medication history (e.g. diuretics, SSRIs, antiepileptics)
    • History of chronic disease (e.g. cirrhosis, heart failure, malignancy)
  • Assess volume status
    • Hypovolaemia: dry mucous membranes, hypotension, tachycardia
    • Euvolaemia: normal volume status (e.g. in SIADH)
    • Hypervolaemia: peripheral oedema, ascites, raised JVP
  • Evaluate neurological status
    • Confusion, decreased GCS, focal deficits, seizures

Red Flags (suggesting acute or severe hyponatraemia)

  • Persistent nausea and vomiting
  • Irritability or agitation
  • Headache
  • Reduced level of consciousness
  • Seizures

Complications

  • Cerebral oedema
    • Secondary to abrupt sodium losses and free water shift from vascular to interstitial space
  • ECG changes
    • Cause of non-ischaemic ST elevation on ECG
  • Pontine demyelinosis (no clear evidence that associated with rapid correction)
    • Develops 3-5 days after treatment
    • Demyelination of central pons, corticobulbar and corticospinal tracts
    • Altered mental state, pseudobulbar palsies
    • Dysphasia and spastic quadriparesis
    • More likely in chronic hyponatraemia

Correction

Depends on rapidity of onset and clinical symptoms

  • Hypovolaemic hyponatraemia
    • may respond to intravenous sodium chloride 0.9%, with potassium supplements if required. 
  • Hypervolaemic hyponatraemia
    • who are oedematous due to heart, liver or kidney failure may respond to fluid restriction. 
    • A loop diuretic may be added as long as the effective intravascular volume is not depleted further
  • Euvolaemic hyponatraemia

is based on:

  • the presence of central nervous system symptoms (unconsciousness, seizure, drowsiness, headache)
  • the severity
  • the rate of development.
  • Mild to moderate in euvolaemic or hypervolaemic patients (serum sodium concentration from 120 to 135 mmol/L, no cerebral symptoms)
    • fluid restriction
      • (eg restrict to 500 mL to 1 litre per 24 hours, or 500 mL less than daily urine output)
      • Monitor serum electrolytes, creatinine and urine output daily or twice daily
  • Severe Hyponatremia
    • serum sodium concentration lower than 120 mmol/L OR
    •  with cerebral symptoms
    • Treat with
      • IV sodium chloride 3% (513 mmol/L)
    • The initial target serum Na should NOT be higher than 120 mmol/L
    • Correction should be:
      • not more than 10 mmol/L in the first 24 hours
      • not more than 18 mmol/L in the first 48 hours.

Calculations:

  • Calculate Na deficit = (desired Na-current Na) x (0.6 x body weight)

Correction

  • In acute severe hyponatraemia, aim for 1-2mEq/hour correction
  • In chronic severe hyponatraemia aim for 0.5-1mEq/hour correction.
  • Hypertonic saline replacement
    • 3% saline (513mEq/L) by giving (deficit/513) to the patient at the rate of 1mEq/hour over 4 hours
  • Rapid correction may lead to pontine myelinolysis
    • Patients with chronic hyponatraemia (ie known duration more than 48 hours) are particularly at risk. Additional factors that increase this risk include:
    • serum sodium concentration lower than or equal to 105 mmol/L
    • hypokalaemia
    • alcoholism
    • malnutrition
    • advanced liver disease
  • More rapid initial correction can be considered in patients with:
    • seizures or coma, regardless of whether the hyponatraemia is known to be chronic
    • self-induced acute water intoxication (eg psychiatric conditions, endurance exercise)
    • known hyponatraemia for less than 24 to 48 hours
    • intracranial pathology or increased intracranial pressure

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