Part II: When "grand mal" seizures don't stop.

It's rare, but sometimes our treatments don't work. Usually it's a sign that we're not treating the right problem.

(This is Part II of a two-part series which began yesterday).

Here's where we left off. My patient had just had a couple of grand mal seizures. But was not waking up quickly enough. He’d received a couple rounds of anti-seizure medications, and it was unclear whether the medications had worked or whether his shaking had stopped spontaneously.

A nurse had entered the room with a new piece of information that made me realize that the patient was probably still having a seizure inside of his brain, but the external signs of that—the intense shaking and clenching of the body’s muscles—had stopped.

He was in “non-convulsive status epilepticus”—seizures that last a long time in which physical convulsions are absent.

What the nurse told me was that one of the lab tests that had been drawn back in triage had been run and immediately flagged as a “panic value.” That meant that the result likely indicated an extremely dangerous situation for the patient.

“Doc, the sodium is 106.”

Oof. That’s a profoundly low level. Most people run in the high 130s-140s. If you’re in the low 130s, it’s not an emergency, and dehydration is usually the cause. Even results in the 120s are seen for a variety of reasons, some of which are self-limited and get better on their own, others are indicative of a problem requiring medical attention.* When we get into the 110s, we start to worry.

Low sodium, or hyponatremia, can cause confusion and lethargy.** It can have all sorts of physical manifestations. The lower that number gets, the more likely a seizure becomes. I’ve never seen a patient have a seizure with a sodium level higher than 114 or so, though I’ve heard of it. I’ve also seen some patients with scary low numbers who did not have a seizure and even some who felt fine at those levels. I can remember a few patients whose sodium levels were hovering above or below 110 who did not have anything close to a seizure. Numbers are not the whole story. They never are.

But if you’re going to have a seizure due to low sodium, a level of 106 would certainly get you there.

Now I knew that our benzodiazepines (the lorazapam, or "Ativan”) I’d given the patient likely had had no effect. Benzos don’t do much for low sodium seizures. The shaking had stopped, but it must have happened spontaneously. The patient was likely still having a seizure inside of his brain, but to an observer, he just looked like a guy lying in a stupor.

To treat a seizure caused by low sodium would take far longer. If we gave him too much sodium right away, we could caused a devastating complication called “locked-in syndrome.” I knew we’d have to give him highly concentrated sodium slowly, over a prolonged period.

He would not be able to protect his airway for that long. His clinical course of unconsciousness was now anticipated to be far longer than your typical seizure patient—who might be awake and talking 15 minutes after even the scariest looking seizure. This patient needed to be on a ventilator, until the problem was corrected.

So I intubated him. I called the ICU and together we agreed on the right amount and rate of sodium chloride to start through his IV.

I sent him up to the ICU and went back to work in the ER. My next patient probably had a sprained ankle, a stomach bug, or needed a couple of stitches.

Emergency medicine is like that. You don’t usually go from one intense situation to the next. Instead, when a high-stakes case wraps up, you often go back and tie up the loose ends from some lower acuity stuff that you’d left behind in order to run to the patient who needed you most.

My mind kept thinking about that case, though. What had caused this? Was it something terrible? I knew I might find out later, but it wasn’t certain.

A week later, I went to sign my chart—which is the last time I open a patient’s medical record. In cases like this, I want to know how his recovery had gone. In this case, I wanted to know why he’d had a hyponatremic seizure.

The causes of hyponatremic seizures are wide ranging, but they are quite rare. (By the way, the answer to yesterday’s quiz question was that strokes are the most common cause of non-convulsive status epilepticus. Epilepsy is not a common reason. That’s because our anti-epilepsy medications tend to work quite well, so patients don’t often reach “status” state.)

In this case, it was determined that the patient had accidentally taken too many medications that lower sodium levels. What had happened made complete sense, but it was a fairly unlucky situation.

Months prior, his doctor had prescribed him a drug to keep his blood pressure down, and decrease fluid retention. That drug lowers your sodium. But it didn’t seem to be working. So the doctor added a second drug on top. After a while, that didn’t seem to be making a dent either. So, the doctor added a third drug. Unfortunately, the patient had not been taking any of the medications up until that point. But once his doctor had prescribed three medications, he told himself, “Okay, the doc seems serious. I’ll start taking my meds now.”

His doctor thought that he had slowly gone from one, to two, to three drugs, in steady succession. In fact what had happened was that the patient had never taken any of the medications, until one day when he started taking all three at once. His body was not accustomed to that level of diuresis, and within days his sodium dropped from the high 130s to 106. That’s why he was in status epilepticus in my ER.

After the patient went to the ICU where his sodium levels were carefully corrected and monitored, he came off of the breathing machine and woke up. This little mystery got solved and he went back to his normal life.

What had caused this? Well, I could ask a kidney doctor to explain that. But that would not explain the real problem. The real problem was one of communication.

For whatever reason, the patient had decided not to take any of the medications that his doctor prescribed and he had not told his doctor that. When his doctor upped the ante and the patient then decided to adhere to the plan all at once, things quickly went to a dangerous place.

Perhaps the doctor could have asked his patient about whether he was taking his medications before adding that third one. Or maybe the doctor did just that, but the patient just didn’t tell him what was really going on. Doctor-patient trust is more important and delicate than we often realize. Either way, a potentially devastating situation had occurred—one which could have been avoided simply through a conversation.

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*By the way, sometimes low sodium is not really low—when glucose levels are extremely high, a low sodium level has to be “corrected.” For example, a patient with a sodium of 120 has a “corrected” sodium of 130 (still low, but a lot safer) if their glucose levels are 500. (Now, having a glucose level of 500 can be a huge problem for other reasons, but that’s another story).

**Another thing: It’s almost impossible to get dangerously low sodium simply by routine dietary changes. It can happen but, please don’t worry about this, unless you have a known kidney, endocrine disease, or some other problem in which dangerous changes in your blood electrolytes is a known problem—in which case, your doctor probably already has provided you guidance.