Physiology
Endocrine
Regarding hypernatraemia, which of the following statements is INCORRECT:
Answer:
Acute severe hypernatraemia is a medical emergency and requires inpatient management in a high dependency setting. Seizures and intracranial vascular haemorrhage as a result of brain cell crenation can occur. The cause is most commonly excessive water loss and the key aspect of treatment is aggressive fluid replacement (typically with normal saline as this is relatively hypotonic). If urine osmolality is low, diabetes insipidus (DI) should be considered and a trial of synthetic ADH given. In patients with known DI, it is essential to ensure synthetic ADH is given parenterally and that close fluid balance is observed.Hypernatraemia
Physiology / Endocrine / Pituitary Function
Last Updated: 21st April 2019
Hypernatraemia is an increase in the serum sodium concentration > 145 mmol/L. It is less common than hyponatraemia in clinical practice but it is a sign of significant disease. Hypernatraemia may arise from either sodium gain or much more commonly from water deficit (both are associated with a raised plasma osmolality).
Causes
Hypernatraemia can be thought of in relation to actual total body sodium:
Hypotonic fluid loss
The most common group of patients are those with hypernatraemia with decreased total body sodium through loss of both water and sodium, but with a greater proportion of water loss which may result from:
- Renal losses e.g. osmotic diuresis secondary to uncontrolled diabetes mellitus, mannitol, or renal disease
- Skin losses e.g. burns, excessive sweating in hot climate or exercise
- Gastrointestinal losses e.g. vomiting, diarrhoea, fistulae
Pure water depletion
Patients with hypernatraemia with normal total body sodium have a pure water deficit which may result from:
- Inadequate water intake e.g. unconscious patient, dementia, disordered thirst perception in hypothalamic lesion
- Extra-renal loss e.g. hyperventilation, hyperthyroidism, mucocutaneous loss
- Renal loss e.g. diabetes insipidus or chronic kidney disease
Salt gain
Hypernatraemia with an actual increase in total body sodium is rare. Mild true hypernatraemia may be caused by primary hyperaldosteronism, but this is not typical. Other causes include acute salt poisoning e.g. intravenous sodium bicarbonate, hypertonic saline, high sodium feeds in infants, near drowning in salt water, salt ingestion.
Assessment and Management
When assessing patients with hypernatraemia:
- If the hypernatraemia is mild (Na ? 150 mmol/L) and the patient has obvious signs of dehydration it is likely the ECF volume is reduced and that the patient has lost both sodium and water. Treatment should aim to replace the deficit of fluid by infusing isotonic saline, or if the deficit is large, hypotonic saline.
- With more severe hypernatraemia (150 - 170 mmol/L), pure water loss is likely if the clinical signs of dehydration are mild in relation to the degree of hypernatraemia - this is because pure water loss is distributed evenly throughout the body compartments and the sodium content of the ECF is unchanged. Treatment should be aimed at replacing water either orally, or with 5% dextrose.
- With gross hypernatraemia ( > 180 mmol/L), an excess of sodium is likely, the patient may present with signs of fluid overload. Treatment may be with diuretics, or rarely, by renal dialysis.
Acute severe hypernatraemia
This is a medical emergency and requires inpatient management in a high dependency setting. Seizures and intracranial vascular haemorrhage as a result of brain cell crenation can occur. The cause is most commonly excessive water loss and the key aspect of treatment is aggressive fluid replacement (typically with normal saline as this is relatively hypotonic). If urine osmolality is low, DI should be considered and a trial of synthetic ADH given. In patients with known DI, it is essential to ensure synthetic ADH is given parenterally and that close fluid balance is observed.
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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 |
