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Time Completed: 02:50:59

Final Score 75%

135
45

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Nephrology

Question 178 of 180

You have been asked to give a teaching session to a group of medical students attached to the Emergency Department. The title of the session is "Electrolyte Disturbance in the ED" and you are discussing hypernatraemia. Which of the following is NOT a typical feature of hypernatraemia?

Answer:

  • Symptoms of hypernatraemia are nonspecific and depend on the underlying cause and the severity. If hypernatraemia is acute (generally defined as onset within <48 hours), the higher osmolality in the extracellular space causes water to move out of brain cells causing the brain to shrink. This shrinkage can lead to neurological manifestations, including lethargy, weakness, and irritability.
  • Signs of hypernatraemia usually involve central nervous system (CNS) manifestations and include irritability, restlessness, muscle twitching, spasticity, and hyperreflexia.

Hypernatraemia

Hypernatraemia is an increase in the serum sodium concentration > 145 mmol/L. Hypernatraemia is a state of hyperosmolality (>295 mmol/kg), and is primarily a result of water deficit or, rarely, sodium gain. Due to the maintenance of osmotic equilibrium, intracellular fluid (ICF) becomes volume contracted. The appropriate responses are increased water intake stimulated by thirst, and the excretion of the minimal amount of maximally concentrated urine.

Causes

  • Free water loss (most common):
    • Renal loss
      • Osmotic diuresis
        • Hyperglycaemia and glycosuria in poorly controlled diabetes mellitus
        • Loop diuretics
        • Increased production of urea (e.g. from a high-protein diet)
        • Intravenous mannitol
        • Post-obstructive diuresis after correction of urinary output obstruction
      • Diabetes insipidus
    • Non-renal loss
      • Insensible losses e.g. fever, exercise, heat exposure, burns
      • Severe diarrhoea
      • Severe vomiting
      • Enteric fistulae
  • Free water intake deficit:
    • Those with limited access to water e.g. infants, disabled people, cognitively impaired people, postoperative patients, nursing home patients, and intubated patients
    • Impaired thirst mechanism as a result of primary hypodipsia
    • Inadequate breastfeeding without supplementation
  • Sodium intake (rare):
    • Inadvertent administration of hypertonic sodium chloride or sodium bicarbonate
    • Replacement of sugar with salt in infant formula (accidental or intentional)
    • Massive salt ingestion
  • Mineralocorticoid excess (causing sodium excess):
    • Cushing's syndrome
    • Primary aldosteronism

Clinical features

  • Symptoms of hypernatraemia are nonspecific and depend on the underlying cause and the severity. If hypernatraemia is acute (generally defined as onset within <48 hours), the higher osmolality in the extracellular space causes water to move out of brain cells causing the brain to shrink. This shrinkage can lead to neurological manifestations, including lethargy, weakness, and irritability.
  • Signs of hypernatraemia usually involve central nervous system (CNS) manifestations and include irritability, restlessness, muscle twitching, spasticity, and hyperreflexia.
  • Severe hypernatraemia (plasma sodium concentration >158 mmol/L) may present with serious signs and symptoms, such as hyperthermia, delirium, seizures, and coma.
  • A thorough physical examination should be completed, including evaluation of volume status, mental status, and neurological assessment. The aetiology is most easily elicited by considering the patient's volume status.
    • Hypovolaemic hypernatraemia (signs of volume depletion, including dry mucous membranes, poor skin turgor, sunken eyes, irritability, tachycardia, hypotension or postural hypotension, decreased urine output, and weight loss) may be caused by renal and non-renal water losses and water intake deficit.
    • Hypervolaemic hypernatraemia (signs of volume overload, including weight gain, peripheral oedema, hypertension, irritating cough, dyspnoea, jugular vein distention, and crepitations on auscultation) may be caused by exogenous sodium intake and mineralocorticoid excess
    • Euvolaemic hypernatraemia may be caused by diabetes insipidus

Investigations

  • Serum sodium
    • A plasma sodium concentration of >145 mmol/L confirms the presence of hypernatraemia.
    • Serum sodium levels of 150-170 mmol/L usually indicate volume depletion and the causes thereof.
    • Serum sodium of >170 mmol/L is usually associated with diabetes insipidus.
    • Serum sodium of >190 mmol/L is usually a result of exogenous sodium gain.
  • Urine osmolality
    • Urine osmolality may help determine the underlying aetiology. Normal kidney response to hypernatraemia is to excrete a minimal amount of urine that is maximally concentrated.
    • Hypertonic urine (>500 mmol/kg) is usually observed with extra-renal fluid losses, as is the case with vomiting, diarrhoea, burns, and excessive sweating.
    • Isotonic urine (200 - 500 mmol/kg) can be seen with diuretic use, osmotic diuresis, and salt wasting.
    • Hypotonic urine (< 150 mmol/kg) associated with polyuria is seen with diabetes insipidus.
  • A metabolic panel, including serum glucose, potassium, chloride, urea, and creatinine, should also form part of the initial work-up to exclude associated electrolyte abnormalities and renal impairment.
  • Specific investigations may include tests for diabetes insipidus, diabetes mellitus, or mineralocorticoid excess.
  • Imaging studies
    • Head CT scan or MRI may reveal a central cause for hypernatraemia and should be performed in all patients with severe hypernatraemia and no occult aetiology. In addition, brain imaging helps to exclude intracranial haemorrhage caused by traction on the dural bridging veins and sinuses as a result of brain shrinkage. Dural sinus thrombosis may occur from the haemoconcentration of total body water loss and can also be detected with head CT scan or MRI. CT scan or MRI of the adrenal glands may reveal an underlying adrenal mass lesion in patients with suspected primary aldosteronism.

Management

  • Treatment should be directed at addressing the underlying cause (e.g. stop offending medication, treat fever, relieve urinary obstruction, give insulin, discontinue sodium sources), as well as replacing any free water deficit and ongoing fluid losses, while monitoring serum sodium concentration to ensure levels are returning to the correct range at the desired rate.
  • Severe hypernatraemia
    • This is a medical emergency and requires inpatient management in a high dependency setting. To avoid cerebral oedema the serum sodium should not be corrected any faster than 0.5 mmol/L every hour.
    • Hypovolaemic hypernatraemia (low total body sodium content)
      • Initial treatment relies on stabilising hypovolaemic patients using isotonic saline. Once the patient is stable, the free water deficit can be corrected orally or with intravenous fluids over 48 hours.
    • Euvolaemic hypernatraemia (normal total body sodium content)
      • Euvolaemic patients can be treated with hypotonic fluids such as 5% dextrose water to correct the free water deficit.
    • Hypervolaemic hypernatraemia (high total body sodium content)
      • Salt should be restricted and hypotonic fluid should be given to correct the sodium abnormality. Hypervolaemic patients may require diuretics in addition to hypotonic fluid correction.

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  • Biochemistry
  • Blood Gases
  • Haematology
Biochemistry Normal Value
Sodium 135 – 145 mmol/l
Potassium 3.0 – 4.5 mmol/l
Urea 2.5 – 7.5 mmol/l
Glucose 3.5 – 5.0 mmol/l
Creatinine 35 – 135 μmol/l
Alanine Aminotransferase (ALT) 5 – 35 U/l
Gamma-glutamyl Transferase (GGT) < 65 U/l
Alkaline Phosphatase (ALP) 30 – 135 U/l
Aspartate Aminotransferase (AST) < 40 U/l
Total Protein 60 – 80 g/l
Albumin 35 – 50 g/l
Globulin 2.4 – 3.5 g/dl
Amylase < 70 U/l
Total Bilirubin 3 – 17 μmol/l
Calcium 2.1 – 2.5 mmol/l
Chloride 95 – 105 mmol/l
Phosphate 0.8 – 1.4 mmol/l
Haematology Normal Value
Haemoglobin 11.5 – 16.6 g/dl
White Blood Cells 4.0 – 11.0 x 109/l
Platelets 150 – 450 x 109/l
MCV 80 – 96 fl
MCHC 32 – 36 g/dl
Neutrophils 2.0 – 7.5 x 109/l
Lymphocytes 1.5 – 4.0 x 109/l
Monocytes 0.3 – 1.0 x 109/l
Eosinophils 0.1 – 0.5 x 109/l
Basophils < 0.2 x 109/l
Reticulocytes < 2%
Haematocrit 0.35 – 0.49
Red Cell Distribution Width 11 – 15%
Blood Gases Normal Value
pH 7.35 – 7.45
pO2 11 – 14 kPa
pCO2 4.5 – 6.0 kPa
Base Excess -2 – +2 mmol/l
Bicarbonate 24 – 30 mmol/l
Lactate < 2 mmol/l
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