Sigh...Is there anyone who can add 2+2 here?

[ERDoc]

There is no right answer. IV fluids have been debated since the early 20th century and every few years a new article pops up that reignites the debate.

[scubanurse]

Doesn't it also kind of depend on the type of dehydration as to whether you would want hypotonic, hypertonic or isotonic?

Like symptomatic hyponatremia would get more of a hypertonic solution like 3% NaCl?

Edited March 10, 2013 by Kate_826

[ERDoc]

No no no. Never give hypertonic saline to someone who is hyponatremic unless they are seizing. If you correct hyponatremia too quickly you will cause central pontine myelinolysis. Dehydration by itself is treated with fluid replacement. If there are electrolyte issues that is where you have to start getting fancier.

[scubanurse]

gotchya... I was just going to a handout I got in wonderful nursing school I have since learned to double check these things...hence why we get orders from smart doctors like yourself first

[ERDoc]

Always glad to help. Let me know when one of those smart doctors joins the site.

[Arctickat]

Sorry Doc, you are of course and always, correct. My concern wasn't with the amount of dextrose my patient was given. It was with the vast quantities of water he'd received. About 3 litres in I probably would have switched to a D10NS or a D10/0.45%S

[ERDoc]

You are correct, those would have been much better options.

[Kiwiology]

This sounds like a poor appreciation of basic physiology (love me physiology)

However, I was taught that the body will seek to maintain plasma normosmolarity and if too much free water is introduced then the body will sense hypo-osmolarity and expel the excess free water as urine?

In fact, here is what I wrote in a uni assignment about it

Atrial natriuretic peptide is an amino acid peptide released from atrial myocytes in response to distension; the most common cause being hypervolaemia and hypo-osmolar plasma (Klabunde, 2007). ANP increases urine output in an effort to achieve normovolaemia and normal extracellular fluid balance by

• Dilating the efferent arteriole of the nephron which increases glomerular filtration rate (Saladin, 2003),
• Acting upon the distal collecting tubule and duct in the nephron to decrease reabsorption of sodium (Guyton & Hall, 2011),
• Inhibiting anti diuretic hormone secretion from the posterior pituitary gland which … (Saladin, 2003) and,
• Decreasing aldosterone secretion from the adrenal cortex, lowering sodium reabsorption in the nephron thus increasing urine output (Rhodes & Tanner, 2003

​Thirst is awareness of the desire to drink water and intends to aid in restoring extracellular sodium balance (Rhodes & Tanner, 2003). Sodium balance is particularly important in ensuring correct extracellular osmolality which is calculated as ECF solute concentration / ECF volume (normal being 300mOsm/Kg or 2 (Na⁺) + (BUN/28) + (glucose/18)). The thirst centre is located in the anterolateral wall of the third cerebral ventricle and is activated by plasma and cerebrospinal fluid osmolality increases (osmoreceptor feedback) as well as increased release of angiotensin II (Guyton & Hall, 2011). When stimulated the thirst centre encourages drinking water by a reflex decrease in secretions from oral salivary glands. The ingested water will diffuse into the plasma through the gastrointestinal system and decrease extracellular fluid osmolality (Levitsky & Raff, 2011).

Anti-diuretic hormone (arginine vasopressin) is a small nine amino acid nonapeptide manufactured in the anterior hypothalamus and stored for release in the posterior pituitary gland. The principal factors influencing release of ADH is plasma hyperosmolality (osmoreceptors) or hypovolaemia (cardiovascular baroreceptors); in fact, the hypothalamus can detect a deviation as small as one per cent from the normal plasma osmolality of 300mOsm/kg (Rhodes & Tanner, 2003). Release of ADH allows for considerable water reabsorption in the renal collecting ducts by increasing permeability to sodium of the K⁺/Na⁺ ATPase (Levitsky & Raff, 2011)

So in theory would plasma hypo-osmolarity = decreased thirst, decreased ADH and increased ANP which would lead to > urine so < free body water, < ECF and cause > IVF to shift to ECF and lower pOsm thus normalising sodium levels in the plasma by increasing %age of Na to total volume?

[Arctickat]

Sounds about right Kiwi, but given the normal urine production levels of 1 - 2 litres per day, and even the ability to produce up to 1 litre per hour; even this attempt to normalise the imbalance would prove difficult given the vast volume of water involved. Especially given the other medical conditions involved.

[mobey]

There are 2 things I always remind my entry level co-workers when discussing I.V. therapy. They have pretty well been said here, but I just feel compelled to put them in bullet form.

1) When using D5W, the body uses the Dextrose and you are left with free water.

2) The ph of NaCl is 5.5

Just a couple of important points that I feel get overlooked sometimes.

According to S.Weingard: There are 3 emergency treatments for hyponatremia: 1) Send labs (if you are in clinical setting) 2) Treat CNS symptoms with hypertonic saline 3) Do nothing.

http://emcrit.org/podcasts/hyponatremia/

I got a question for ya though: Could/Should Arcticat treat this patient with Normal Saline while transporting to the city?

(I have NO idea if he did or not..... this is NOT an excersise in judging my Sk brother, just getting some juices flowing amongst my peers)