83. Hyperosmolarity, hypertonicity. Forms, causes, consequences
The osmotic pressure (osmolarity) of all water compartments in the body is around 280 – 300 mOsm/kg. Because it’s the same in all compartments is the body normally isotonic or normotonic.
The target for osmoregulation isn’t to regulate the number of osmoles, it’s to regulate the level of water. We have osmoreceptors in the hypothalamus. When the body is hypertonic will water leave the cells and enter the interstitium, causing the cells to shrink. These osmoreceptor cells can sense this change in size. When they shrink will they produce more ADH, when they swell will they produce less. These cells therefore respond to hypertonicity by producing more ADH and respond to hypotonicity by producing less ADH. ADH has two important functions here: it increases the thirst sensation in the brain, and it increases water retention in the kidney.
In hypertonicity will ADH increase which causes the body to drink water and excrete less water, which increases the amount of water in the body. This decreases the osmolarity, but the number of osmoles stays the same. The opposite happens in hypotonicity.
We often use the terms hyperosmolarity and hypertonicity interchangeably because an increase in osmolarity almost always causes hypertonicity. The only exception is when the increased osmolarity is due to increased levels of a substance that can enter cells freely, like urea, ethanol or methanol.
Hyperosmolarity
Hyperosmolarity and hypertonicity can be caused by:
- Excessive intake of salt
- Other osmotically active substances (mannitol, sorbitol, X-ray contrast agents)
- Diabetes mellitus
- Diabetes insipidus
- Loss of hypoosmolar fluid, like sweat
Many of these causes have been seen before, as they cause hypervolaemia or hypovolaemia.
Excessive salt intake is well tolerated in healthy adults, but not in young children and people with oliguria.
Diabetes insipidus is the condition where ADH is deficient. The body can’t retain as much water and therefore loses water.
Diabetes mellitus is characterised by hyperglycaemia, which is osmotically active.
Sweat is hypoosmolar.
Compensation and consequences
The body responds to hyperosmolarity by increasing thirst and ADH release, and possibly by decreasing aldosterone secretion.
The consequences depend on whether the hyperosmolarity develops acutely or chronically.
In an acute increase will the brain cells shrink, which causes vessels to stretch, potentially causing bleeding.
In a chronic increase will the brain cells compensate by producing intracellular osmotically activate substances called idiogenic osmoles that counteract the increased hyperosmolarity of the interstitium. This prevents the cells from shrinking, but it also inhibits intracellular enzymes, which isn’t good.
Chronic hyperosmolarity must be corrected slowly to allow the brain cells to get rid of the idiogenic osmoles, or else there will be swelling and brain oedema. Isotonic saline should be given in a slow infusion.