Jump to content

Recommended Posts

Posted
Good, we will most likely need to administer hypertonic saline. I think diuretics would also be a good therapy to consider. So, how quickly are we going to administer the hypertonic saline and when do we start backing off, or do we normalize serum sodium?

When considering the cause, think about the patients respiratory symptoms.

Take care,

chbare.

I mentioned Lasix earlier, but not sure of adm. rate. I might have missed something, but how is his I & O's without diuretics? And after?

  • Replies 49
  • Created
  • Last Reply

Top Posters In This Topic

Posted

A good point. We would need to place a foley and monitor I/O very closely. His urinary output would be quite scant prior to diuretics. Our dose of lasix will vary, and we will need to be very careful about additional electrolyte imbalances when giving lasix.

While I think lasix is a good idea, it will take time to work and this guy needs his seizure activity and cerebral edema controlled, so emphasizing hypertonic saline replacement will be a key treatment. However, just how aggressive will we get with the hypertonic saline? Can we anticipate any problems if we are too aggressive?

Take care,

chbare.

Posted
A good point. We would need to place a foley and monitor I/O very closely. His urinary output would be quite scant prior to diuretics. Our dose of lasix will vary, and we will need to be very careful about additional electrolyte imbalances when giving lasix.

While I think lasix is a good idea, it will take time to work and this guy needs his seizure activity and cerebral edema controlled, so emphasizing hypertonic saline replacement will be a key treatment. However, just how aggressive will we get with the hypertonic saline? Can we anticipate any problems if we are too aggressive?

Take care,

chbare.

That's pretty much what I was trying to get at. Adm. rate of any diuretic is also a key. The hypertonic saline is a must. What about Dilantin? I don't think that was mentioned yet. But I could have missed it.

Posted

We will want to induce diuresis, so, you may end up loading with 40-80mg IV. I suspect this will vary from provider to provider however.

You may want to consider other antiseizure medications; however, we know what is causing the seizures. If we treat the problem, we treat the seizures. We have an intubated patient, so we should be using generous doses of benzos in any event. I would start the hypertonic saline and see if we could control the seizures with that treatment and the benzos that we are giving for sedation. (That will have the inadvertent effect of decreasing seizure activity) However, the priority will still be to treat the cerebral edema.

Any thoughts on the cause? A pituitary tumor is a good guess and one of the causes of SIADH.

Take care,

chbare.

Posted

Small cell lung CA causing an inhibition of water excretion

Posted

Nailed it , small or oat cell carcinoma of the lung.

Take care,

chbare.

Posted
Small cell lung CA causing an inhibition of water excretion

You smart. 8)

Posted

Thank you everybody. I hope you enjoyed this scenario.

Take care,

chbare.

Posted
Thank you everybody. I hope you enjoyed this scenario.

Take care,

chbare.

Keep 'em comin'. :thumbup:

  • 3 weeks later...
Posted

Great scenario, much is to be learned here. Concerning the hyponatremia, this patient is gravely depleted. Loop diuretics and usually 3% hypertonic saline are used to correct this aggressively but very carefully as serum sodium must be raised slowly and precisely, usually occurring over several days. Raising the level too quickly may cause CNS lesions, particularly demyelination of the lower and mid-brain which can lead to devastating neurological deficits, some of which may not be immediately obvious but are usually permanent. Paralysis, dysphagia, dysarthria, or in the worst case scenario, what is known as locked-in syndrome. This patient may present with signs similar to advanced ALS. The patient is unable to move, speak, swallow, or breath unassisted; however their consciousness and intellect remain intact and may only be able to communicate by eye movement. Less devastating lesions may be seen in chronic alcoholics. Interestingly, hyponatremia is also seen in patients who have had a subarachnoid hemorrhage, and occurs through a process known as cerebral salt wasting syndrome. You'll notice in the acute stages these patients are sometimes urinating all over the bed in the ED before the nurse can get a foley in. I'm not entirely up to steam on any of these syndromes but I think there is some good information here, so perhaps the OP or one of the doctors or anyone who is more knowledgeable could enlighten us some more.

I've found a wealth of knowledge can be obtained when you know the disposition of your patient while in-patient or upon their discharge. Just to be able to see some tangible lab results or read the CT dictation and contrast the patients actual diagnosis to your own clinical judgment is invaluable. If ever given this opportunity, such as working in a ER, reading up on some hematology and understanding the radiology concepts beyond what your paramedic school offered will help. Unfortunately, we are not granted this opportunity enough in EMS. We're the skid marks under the hospital. I understand some systems allow follow-ups on all patients, or pertaining to interesting or emotionally charged cases, especially flight services. I think opportunities like this in our line of work would allow for unyielding learning opportunities, but subject for another discussion.


×
×
  • Create New...