Sodium-Na (Hypernatremia, Hyponatremia)

We’re gonna talk about sodium. We’re gonna talk about what sodium is, what it does in the body, and how we can assess hypo and hypernatremia, and what we’re gonna do to correct those issues.

First of all, sodium, the golden rule, the number we’re looking for is 135 to 145 milliequivalents per liter. We’re gonna see it written in a lab value skeleton right up here. So, you might have 132 written right there. That means your sodium level is 132. Now, sodium is our most abundant extracellular cation. That means it’s mostly outside the cell and it’s a cation, so it is positively charged ion. You might see a little bit here in the cell. This is our vessel right here.

One of its main things that it does is it controls fluid distribution between intracellular fluid and extracellular fluid. So, what we have here is we have inside our vessel, we have our solvent and we have sodium, that’s our solute. What sodium’s gonna try to do, it’s gonna try to balance how much solute is dissolved in the solvent. That’s really where we’re really gonna get our osmolarity of our blood. If we have a bunch of fluid outside the vessel, sodium’s gonna move out there to try to balance that out. If we have a lot of fluid inside the vessel, sodium’s gonna try to move in and balance that out. That’s kind of what sodium tries to do. It also plays a big role in muscle contraction and nerve impulses.

Let’s talk about some of the causes of hyponatremia. We have actual causes and we have relative causes. First of all, with the actual causes, we have sweating, wound drainage, low sodium diet diuretics, specifically sodium wasting diuretics like thiazide and loop diuretics. We’re also gonna have hypoaldosteronism as another cause of hyponatremia. Some of your relative causes are SIADH. With SIADH, we’re not getting rid of fluid, so because we’re not getting rid of that fluid, sodium, there’s now less sodium in relation to all the fluid that we’re retaining inside of our body.

Now with water intoxication, it’s the same thing. We’re retaining all this fluid, and so the sodium becomes less dense inside our fluid. Freshwater submission, psychogenic polydipsia. With psychogenic polydipsia, you have these patients you just can … they have extreme thirst and it’s completely insatiable. They might stick their mouth under a faucet and just drink and drink and drink. The problem is this can lead to patients into heart failure. Then there’s also hypotonic fluids. If there’s low tenacity in the fluids, then we’re going to see less sodium inside our body in relation to the fluid.

What are some of the symptoms? If our patient does have hyponatremia, what are the things we’re going to see? First is neuro. I want you to really pay attention to these neuro changes. With these neuro changes, you’re going to see behavioral changes. We’re also going to see increased intracranial pressure. Now that increased intracranial pressure is gonna lead to cerebral edema. If we have cerebral edema, that could lead to seizures. Now this has everything to do with fluid shifts that happens because of the hyponatremia. The fluid shifts out of the vessels and into the brain tissue. So, if it’s all this fluid shifting out, that’s gonna lead to the cerebral edema. If we have that cerebral edema, we’re at risk for seizures. This is not good. That’s why in our patients with hyponatremia, they got all this sodium out here. This fluid’s coming out after it. So, really monitor your patient’s neuro status if they have hyponatremia.

Musculoskeletal wise, we’re gonna see weakness, especially respiratory wise, our respiratory muscles, and we’re gonna see decreased deep tendon reflexes, DTRs. GI wise, we’re gonna see hyperactive bowel sounds. We’re gonna see nausea, vomiting, diarrhea, and we also might see our patients with cramps. Now, this is due again to fluid shifting out of the vessels and into the GI tract. Cardiovascular wise, this depends entirely on fluid volume status. It depends on the sodium issue. For example, if our patient has hypovolemia, so they have their blood vessel here, but they don’t have a lot of volume in there, what are we gonna see with that? Well, they don’t have a lot of volume, our pulse is gonna become really weak. Our blood pressure’s gonna drop. Our heart rate is gonna go up, to try to push the little bit of fluid that we have around the body. We’re gonna become hypotensive because we’re not getting oxygen to the brain. We’re gonna be dizzy. So, this has a lot more to do with our volume status than our sodium as much.

Now, if the patient has hypovolemia, so here’s their vessel. It’s got just a ton of fluid in here. It’s full. What’s the patient gonna look like? Well they’re gonna have bounding pulses. They’re gonna have a strong blood pressure. That’s how we can watch cardiovascular wise what’s going on with our patient who has hyponatremia. How are we gonna treat this? The first thing I want you guys to do is I want you to remember that you must replace sodium very slowly. We want to avoid fluid overload due to fluid shifting, as we start replacing this. One thing we’re trying to prevent here is something called CPM, or Central Pontine Myelinolysis. What is that? That’s really neuro damage that occurs due to overcorrection of hyponatremia. You might have heard of something called Locked-in syndrome. That’s what CPM is. CPM is this Locked-in syndrome due to overcorrection of our hyponatremia.

Now, sodium levels, you should only be increasing sodium levels by 0.5 milliequivalents per liter per hour max. In a 24 hours period, you should only increase it by 12 points. Now you’re also likely, and you should be doing this, is checking your sodium levels every two to four hours. We can also stop giving sodium wasting diuretics. We give IV fluids. We give 0.9% NaCl. If they’re hypovolemic, we want to ensure good intravascular volume before we start trying to correct this too much. So, we get their volume where it should be, then we can start working on the sodium. Now then we can start giving hypertonic saline or 3% NS. We don’t want to give osmotic diuretics where they can lose some of this H2O without losing the sodium. We want to retain that sodium if they’re hypovolemic.

Now for dietary changes, we’re gonna try to increase their sodium intake, and then we want to do a free water restrictions. This means they can’t have any H2O from any source. No tea, no soda, no juice, no coffee, nothing, no water. This gets very, very hard for your patient, but we’ve got to correct this hyponatremia.

Now, let’s talk hypernatremia. Some of the actual causes for hypernatremia are steroids. This causes the kidneys to retain sodium. Then there’s oral ingestion. Do they take a bunch of sodium? There can also be hypertonic saline. Maybe they’re taking 1.5 NS, 3%, or even 5% NS. That’s gonna cause sodium to go up, and that’s again why we’re correcting it very slowly. If they’re hypo, and they have Cushing’s Syndrome as well, it’s gonna cause the kidneys to retain sodium. Some of the relative ones, of course, NPO, they’re not eating or drinking, so their sodium’s gonna rise in relation to the fluid volume. Then maybe a fever, hyperventilation. If you put your hand in front of your mouth and just breathe, you can feel a little bit of that insensible loss, that moisture in the air that you breathe out, dehydration. Again, less fluid, so sodium looks like it’s higher in relation to the fluid that you have. And then infection as well.

Some of our symptoms for our patients who have hypernatremia, elevated sodium levels, are neuro. Again, thinking about neuro a lot when we think about sodium. This is related to cellular dehydration in the brain cells. Fluid shifts out of the cells, into the vessel, so here goes our sodium shifting out of the cell into the vessels to try to balance out sodium levels. Our cell is gonna get a little bit dehydrated there. If the patient is hypovolemic, they’re gonna get irritable, they’re gonna be confused, they might even get manic, and they’re very, very cranky. If they’re hypervolemic, they’re gonna become lethargic, drowsy, stupor. This could even lead to a coma. You can see how critical it is, whether it’s hypo or hypernatremia, that you’re monitoring sodium levels and monitoring your patient very closely.

Musculoskeletal wise, watch for twitching, cramps and weakness. Cardiovascular, the patient’s gonna have decreased contractility. If they’re hypovolemic, same thing here. We’re gonna start seeing these symptoms based on fluid volume status. If the patient is hypovolemic, so not a lot of fluid in there, we’re gonna see a decreased blood pressure, weak pulses. Again this is a lot due to the symptoms of the hypovolemia. If they’re hypervolemia, again same things we talked about, increased blood pressure, JVD, jugular venous distention, bounding pulses. Other things we’re gonna see are signs of dehydration, extreme thirst, dry mucous membranes, dry hot skin. Remember, hypernatremia causes cellular dehydration.

Now, how are we gonna treat hypernatremia? It’s important to know how we’re gonna treat our patient with this. We want to bring sodium levels down very slowly. Overcorrection can lead to seizures, as we talked about before. Now, we can give hypertonic fluids, fluids like half NS, or D5W. If they’re hypervolemic, then we can give sodium wasting diuretics. Now we want to discuss with a dietician. We want to talk to a dietician about setting up a sodium restricted diet. How can we get this patient to be eating a good healthy diet without eating too much sodium? And we can talk to them about increasing free water. This helps dilute the blood and bring levels down, but we can give them even, like if the patient has an NG tube, we can actually give them tap water bolus flushes in their NG tube if they one, if that’s something that’s available.

Now, let’s touch on the key points with sodium. Again, it’s a value of 135 to 145 milliequivalents per liter. The main functions are it plays a role in fluid balance, nerve impulses and muscle contraction. Keep in mind that for hyponatremia, there are actual causes of sodium losses or relative hyponatremia because of increased fluids. This can lead, and the biggest concern we have here with these patients, is it can lead to cerebral edema, which causes increased ICP and can lead to seizures. Remember that we have to replace sodium very slowly, usually using hypertonic saline, to prevent CPM, as we talked about, our Locked-in syndrome. With hypernatremia as well, we can have actual versus relative, as the cause for the hypernatremia. We’re gonna look for dehydration everywhere, but really the big place we’re gonna look for this is especially in the brain.

With this, we can replace with hypotonic solutions and we can give free water as well to help these patients. This patient is going to be very cranky. We want to again replace and fix very, very slowly. Our top priority with this is to treat the cause. Find the cause, treat the cause. In the case of sodium changes, we see that the brain and nervous system are most affected, so we want to monitor neuro status and protect the brain as much as we can.

All right, guys. That is sodium. I hope that helps. Hope that helps clear it up a little bit in your minds. As we always say here, go out and be your best selves today. Happy nursing.