In this section : Electrolyte Disturbances
Hyperkalaemia
Hypomagnesaemia
Hypophosphataemia
Hypernatraemia
Hypokalaemia
Hyponatraemia
Hypocalcaemia
Hypercalcaemia
Hypernatraemia
Last updated 26th April 2024
Mechanisms
- Hypernatraemia is a state of hyperosmolality. It primarily occurs as a result of water deficit or, more rarely, sodium gain.
- Hypernatremia is uncommon because the ensuing rise in plasma osmolality stimulates the release of both ADH and thirst, thereby minimizing further water loss and increasing water intake.
- In adults, it is most often due to water losses in older patients that are not replaced because of impaired mental status
Causes
- Reduced water intake:
- Commonest cause is insufficient water intake in elderly with cognitive impairment
- Hypothalamic lesions impairing thirst or osmoreceptor function
- Free water losses:
- Central or nephrogenic diabetes insipidus (now called ADH deficiency or resistance)
- Osmotic diuresis eg glucose in uncontrolled diabetes mellitus
- Insensible & sweat losses e.g. in fever, exercise, severe burns
- Gastrointestinal losses
- Excess sodium intake or administration of hypertonic sodium solutions
Clinical Features
- Symptoms occur because water moves out of the brain (mirror image of hyponatraemia)
- Symptoms are uncommon in chronic hypernatraemia (the common form of hypernatraemia) and only likely if hypernatraemia is acute
- Symptoms of hypernatraemic dehydration include lethargy, weakness and irritability. If severe, manifestations can include seizures, and coma.
Investigations
- Check the drug list to make sure desmopressin hasn’t be inadvertently stopped- Untreated ADH deficiency ( formerly known as Diabetes Insipidus) has resulted in preventable deaths
- Full electrolyte panel with glucose, calcium, urea and creatinine to assess for presence of uncontrolled diabetes mellitus, other electrolyte abnormalities, renal impairment.
- Measurement of serum and urine osmolality may give further clue to cause.
- If urine osm < plasma osm, consider diabetes insipidus (ADH deficiency/resistance)
- If urine osm > plasma osm, pure volume depletion not due to diabetes insipidus eg inadequate water intake, GI or insensible losses.
General Management
- Treatment should address the underlying cause (e.g. stop offending medication or fluids, treat fever) as well as replacing any free water deficit.
- Fluid replacement strategy is based on severity, volume status (hypo, hyper or euvolaemic), and duration of hypernatraemia (chronic if >48 hrs or unknown, acute if <48 hrs)
- Nearly all patients with hypernatremia will have chronic hypernatraemia, even those who present with acute changes in mentation who are discovered to have hypernatremia.
- Acute hypernatraemia is uncommon, occurring in patients with salt poisoning; in patients with ADH deficiency (diabetes insipidus) who acutely lose the ability to replace their water losses (eg, a patient with ADH deficiency (diabetes insipidus) who undergoes surgery and does not receive adequate intravenous water).
- The key is regular monitoring of serum sodium and adjusting the fluids accordingly.
Fluid Replacement
- Mild cases of hypernatraemia – replace missing body water with oral water (not electrolyte drinks) or glucose 5% IV.
- Severe cases of hypernatraemia eg Na >170mmol/L, give glucose 5% IV unless the patient is volume depleted and hypotensive, in which case give sodium chloride 0.9% IV before water replacement.
- It is important that the rate of reduction of serum Na does not occur more rapidly than about 10mmol/L per day.
- Reassess and record patient’s blood results and clinical conditions every 8 hours. Recheck serum Na after 2 L of fluid replacement, or after 8 hours at the latest.
- Patients should be handed over to the next shift to clarify monitoring and fluid requirements.
- If diabetes is simultaneously present, then BM monitoring is required and if the blood glucose is >30mmol/L then follow the Hyperglycaemic Hyperosmolar Guideline
- In complex cases, the free water deficit can be calculated and advice can be sought from Biochemistry to guide the rate of water replacement.
What Rate of Infusion?
- In acute (<48 hrs) – 3-6ml/kg/hour, aiming to correct sodium to near normal values within 24 hours. If severe symptoms – correct sodium by 2mmol/l/hour in first few hours followed by correction rate of 0.5mmol/l/hour
- In chronic (>48 hrs or unknown duration) – 1.35ml/kg/hour, aiming to correct sodium no faster than 0.5mmol/l/hour or 10-12 mmol/l/day
Hypernatremia Due to Correction of Severe Hyperglycaemia
- Serum sodium rises because of osmotic shift of water from extracellular fluid into cells and because of loss of electrolyte-free water in the urine as excess glucose is excreted.
- Because most of these patients are hypovolemic and hyperglycaemic, free water is usually administered as saline 0.45% at 6-12ml/kg/hr rather than dextrose 5%.
Content by Tina Grant. Updated by Chris Isles.