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Posted
Ok I am probably right off base here but the statement of unable to pee can be different that unable to create pee. So Im going with a blockage or detachment of the bladder. If you cant get rid of urine all sorts of things can happen.

However, this patient has limited urinary output, or we would not have lab studies performed on the urine. I suspect the cause is endocrine in nature.

Take care,

chbare.

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Posted

So her kidney's appear to be functioning properly. But that Na is low. Hyponatremia can be classified as hyper-, hypo- or euvolemic. We now have to figure out which one she is. The FENa also helps. The OP has given us the answer, but the question is why?

Posted

From eMedicine (the complete article is at: http://emedicine.medscape.com/article/767624-overview)

Causes

Hypovolemic hyponatremia develops as sodium and free water are lost and replaced by inappropriately hypotonic fluids, such as tap water, half-normal saline, or dextrose in water. Sodium can be lost through renal or nonrenal routes. Nonrenal routes include GI losses, excessive sweating, third spacing of fluids (eg, ascites, peritonitis, pancreatitis, burns), and cerebral salt-wasting syndrome.

Excess fluid losses (eg, vomiting, diarrhea, excessive sweating, GI fistulas or drainage tubes, pancreatitis, burns) that have been replaced primarily by hypotonic fluids

Acute or chronic renal insufficiency, in which the patient may be unable to excrete adequate amounts of free water

Salt-wasting nephropathy

Cerebral salt-wasting syndrome seen in patients with traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial surgery. Cerebral salt-wasting must be distinguished from SIADH because both conditions can cause hyponatremia in neurosurgical patients, and yet the pathophysiology and treatment are different.4

Prolonged exercise in a hot environment, especially in patients who hydrate aggressively with hyposmolar fluids during exertion. Severe symptomatic hyponatremia has been reported in marathon runners and in recreational hikers in the Grand Canyon.

Euvolemic hyponatremia implies normal sodium stores and a total body excess of free water. This occurs in patients who take in excess fluids.

Psychogenic polydipsia, often in psychiatric patients

Administration of hypotonic intravenous or irrigation fluids in the immediate postoperative period

In a recent meta-analysis, administration of hypotonic maintenance intravenous fluids to hospitalized children has been associated with an increased incidence of acute hyponatremia compared with administration of isotonic maintenance fluids.5

Infants who may have been given inappropriate amounts of free water

Ingestion of sodium phosphate or sodium picosulfates and magnesium citrate combination as a bowel preparation before colonoscopy or colorectal surgery6

SIADH

Hypervolemic hyponatremia occurs when sodium stores increase inappropriately.

This may result from renal causes such as acute or chronic renal failure, when dysfunctional kidneys are unable to excrete the ingested sodium load. It also may occur in response to states of decreased effective intravascular volume.

History of hepatic cirrhosis, congestive heart failure, or nephrotic syndrome, in which patients are subject to insidious increases in total body sodium and free water stores

Uncorrected hypothyroidism or cortisol deficiency (adrenal insufficiency, hypopituitarism)

Consumption of large quantities of beer or use of the recreational drug MDMA (ecstasy)

Hyponatremia can be caused by many medications. Known offenders include acetazolamide, amiloride, amphotericin, aripiprazole, atovaquone, thiazide diuretics, amiodarone, basiliximab, angiotensin II receptor blockers, angiotensin-converting enzyme inhibitors, bromocriptine, carbamazepine, carboplatin, carvedilol, celecoxib, cyclophosphamide, clofibrate, desmopressin, donepezil, duloxetine, eplerenone, gabapentin, haloperidol, heparin, hydroxyurea, indapamide, indomethacin, ketorolac, levetiracetam, loop diuretics, lorcainide, mirtazapine, mitoxantrone, nimodipine, oxcarbazepine, opiates, oxytocin, pimozide, propafenone, proton pump inhibitors, quetiapine, sirolimus, ticlopidine, tolterodine, vincristine, selective serotonin reuptake inhibitors, sulfonylureas, trazodone, tolbutamide, venlafaxine, zalcitabine, and zonisamide.

  • 4 weeks later...
Posted

"Hypervolemic hyponatremia occurs when sodium stores increase inappropriately."

I don't get this. Wouldn't this by hypernatremia?

Posted
The college med school lab is at your disposal should you request it.

Has anyone established if the patient visited said lab for "samples" of meds, such as "X", or other sick bird recreational pharmaceuticals?

(Sick Bird= Ill Eagle, or illegal)

Posted

Could be MDMA, although more indicitive of PMA.

PMA tends to have this reaction moreso than MDMA.

Also the use of

Maxeran. (Reglan for your southern mates, or Maxolon in other countries.)

in a 20 year old female, especially in this condition needs to be measured & seriously not considered due to the Dystonic reactions that are evident in Females under 21. There is also conjecture to the efficacy of this drug. Also, if she has swallowed something, Metoclopromide, the generic name for this drug, has an action of upper GIT motility, do you really want to be pushing it through, or are we better to place her lateral & let her vomit to expell anything that is left?

Posted
"Hypervolemic hyponatremia occurs when sodium stores increase inappropriately."

I don't get this. Wouldn't this by hypernatremia?

I suppose so yes ... wiould make logical sense!

Could be MDMA, although more indicitive of PMA.

PMA tends to have this reaction moreso than MDMA.

Also the use of

in a 20 year old female, especially in this condition needs to be measured & seriously not considered due to the Dystonic reactions that are evident in Females under 21. There is also conjecture to the efficacy of this drug. Also, if she has swallowed something, Metoclopromide, the generic name for this drug, has an action of upper GIT motility, do you really want to be pushing it through, or are we better to place her lateral & let her vomit to expell anything that is left?

Metaclopramide (maloxon) is a nasty, cheap, shitty anti emetic, it can cause whacky dystonic reactions and from what I've seen is not very good. I've seen good results with zofran but anyway .... I'd rather drop an NG tube or leave her be.


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