USMLE FA 2012 P525: Osmotic Diuretic

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FA says that one of the clinical uses for mannitol (an osmotic diuretic) is for treating shock. Why?

Mannitol is an osmotically active solute that causes fluid shifts between compartments. Mannitol administration will result in a rise in plasma osmolality which will pull fluid from the ICF to the ECF and thus increase plasma volume. If you were to infuse normal saline into the vascular compartment, only ~1/3 would stay there. I suppose the theory with mannitol use is that, since it doesn't cross membranes, you get more fluid movement and thus more rapid volume resuscitation.

I haven't ever heard much about mannitol in shock so that's a pretty cursory explanation of my understanding of the theory. In real life, I feel like you would risk cellular shrinkage and something akin to central pontine myelinolysis could occur (similar to what happens with rapid infusion of 3% Saline), but I'm not sure on that one.

Hope that helps.

Edit: ehh I'm not so sure now. FA says that mannitol causes increased tubular fluid osmolarity and it increases urine flow. FA also says that if you administer too much it will cause dehydration. Typo on the "treatment of shock" part?

Mannitol is injected into the bloodstream, used mostly for treated raised ICP. It can be filtered by the kidneys but will not be reabsorbed.

Now do you see why it can be both a diuretic AND treat hypovolemic shock AND raised ICP?

The clinical significance of continuous intracarotid infusion of a small dose of mannitol (ICI of mannitol) was discussed. Eighteen patients suffering from severe head injury with Glasgow coma scale (GCS) less than 6 were treated by ICI of mannitol for the improvement of raised intracranial pressure (ICP). In all of these 18 cases, conventional venous administration of mannitol could not be carried out, because of the unstable vital signs due to hypovolemic shock such as multiple trauma or disturbance of serum sodium and potassium levels. This method requires that a 20% mannitol solution be directly and continuously administered to the bilateral common carotid artery. The ICP 6 hours after the beginning of ICI of mannitol was significantly lower than the ICP just before the treatment. The total amount of excretion of the sodium and potassium through the urine every hour decreased significantly after this method was used. It was also noticed that this method was very suitable for stabilizing the vital signs in cases which had unstable vital signs such as hypovolemic shock. These findings suggested that ICI of mannitol has an advantage over the conventional venous administration of mannitol in cases which had to have correction of serum electrolyte or which had unstable vital signs.