Hypertonicity: Clinical entities, manifestations and treatment

Table 1 Body sodium and water changes leading to hypernatremia

Nae	Body H2O	Clinical example
↔	↓	Diabetes insipidus
↑	↔	Salt tablet ingestion
↑↑	↑	Hypertonic infusions containing sodium salts
↓	↓↓	Loop diuretics, excessive sweating, osmotic diarrhea, osmotic diuresis
↑	↓	Not seen in practice

Na_e: Exchangeable body sodium; ↓ = decrease; ↓↓ = greater decrease; ↑ = increase; ↑↑ = greater increase, ↔ = no change.

Table 2 Clinical states causing hypernatremia from inadequate water intake

Lack of water sources

Subject lost in desert

Inability of patient to drink water or ask for it

Tracheal intubation and sedation

Dementia

Delirium

Paranoia

Severe depression

Adipsia or hypodipsia caused by central nervous system disorder compromising the neural pathways of thirst

Granulomas, e.g., sarcoidosis

Tumors, e.g., craniopharyngioma, seminoma, lymphoma, astrocytoma

Degenerative processes, e.g., Parkinson’s disease

Congenital syndromes, e.g., ectodactyly-ectodermal dysplasia- cleftlip-palate syndrome

Diabetes insipidus (a fraction of the patients)

Table 3 Clinical states causing excessive water loss

Extrarenal water loss

Gastrointestinal losses

Vomiting

Nasogastric drainage

Ileostomy

Pancreatobiliary fistula

Diarrhea (non-secretory)

Laxatives, e.g., lactulose

Skin

Excessive sweating

Respiratory airways

Hyperpnea

Tracheal intubation

Mechanical ventilation

Excessive renal water losses

Osmotic (solute) diuresis

Osmotic diuretics, e.g., mannitol

Glucosuria, e.g., hyperglycemia, sodium-glucose transporter 2 (SGLT2) inhibitors

Urea diuresis, e.g., diuresis post-acute tubular necrosis, post- obstructive diuresis, use of catabolic medications (corticosteroids, tetracyclines, etc.), high protein intake, urea treatment for hyponatremia

Salt diuresis, e.g., intravenous infusion of saline, high salt intake

Water diuresis

Central diabetes insipidus

Idiopathic (most common)

Genetic: Familial (mutation causing misfolding of vasopressin), congenital hypopituitarism, Wolfram syndrome (diabetes insipidus, diabetes mellitus, optic atrophy, deafness)

Acquired: Neurosurgery, head trauma, brain tumors, infiltrative disorders (sarcoidosis, Langerhans cell histiocytosis, etc.)

Nephrogenic diabetes insipidus

Genetic: Inactivating mutations of V2 receptor gene (most common) or aquaporin 2 gene

Acquired:

Renal disease (chronic renal failure, post-acute tubular necrosis, obstructive nephropathy, sickle cell disease, autosomal dominant polycystic kidney disease)

Electrolyte disorders: Hypokalemia, hypercalcemia

Drugs: Lithium, amphotericin, demeclocycline, ifosfamide, V2 receptor antagonists

Gestation: Increased placental production of vasopressinase

Upward resetting of the osmostat (reset osmostat): Primary hyperaldosteronism (thought to be secondary to volume expansion and resulting in modest hypernatremia, up to 147 mmol/L)

Table 4 Electrolyte composition of various gastrointestinal fluids

Fluid source	Sodium (mmol/L)	Potassium (mmol/L)
Vomiting, nasogastric drainage	20-100	10-15
Secretory diarrhea	40-140	15-40
Non-secretory diarrhea	50-100	15-20
Adapted ileostomy	40-90	5
New ileostomy	115-140	5-15
Sweat	38-45	5

Data obtained from ref. [21].