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Altered LOC: What’s the cause?

In the pre-hospital arena, as well as in the ER, we see sufficient numbers of patients with diabetes. While we think we can easily recognize the symptoms, it can sometimes be a bit tricky. Here’s an interesting case that shows us one of the extremes of this common disease.

Last week the ALS Unit was called to the apartment of a 24-year-old male college student for altered LOC. A friend had called 911, telling operators that the patient wasn’t acting normally. With the arrival of the ALS team and upon questioning the friend, the medics attempted to ascertain clues that could lead them to a differential diagnosis. Unfortunately, all of their questions about prior history, drug use, etc. were met with the same answer of, “Duhhh, I don’t know.” No pills or bottles were found at the scene.

The medics did a stand-up job of following their ALOC protocol by checking vitals and blood sugar (which was high). The patient had dry skin, tachycardia, rapid breathing, and seemed “out of it.”

When the paramedics arrived in my ER, I asked them what they thought could be occurring. They were right on target, mentioning a number of possibilities in their differential diagnoses: heat illness, drugs, DKA, and sepsis, to name a few. They then asked me a good question: how was I going to sort things out?

The real answer is that I purposely never start off 100 percent sure of my diagnosis. It keeps me thinking about other disease possibilities. To start, I also consider toxins, poisons, or other metabolic problems. Each new bit of information acquired either increases or decreases my confidence. (The logisticians call this “fuzzy logic.”) Here are a few of the bits of information I received, and how they helped.

History — I didn’t get anything from the patient. No pills or bottles were found at the scene, so there is a diminished chance that the diagnosis would involve a toxin.

Physical — We check the patient’s temperature (afebrile), which makes sepsis slightly less likely. (In bad sepsis, it’s possible to not have a fever.) The elevated pulse, dry mouth, and slightly low BP all point towards volume depletion, while the tachypnea is a clue for an underlying toxic problem or acidosis. This pointed me a little more towards a metabolic problem, like DKA, but this too could apply to toxins.

Labs — Lab results indicate high blood sugar (>900), elevated K (potassium) (>7), and elevated BUN and creatinine. Blood gas results show a metabolic acidosis (<7.0) with a respiratory compensation, and white blood cell count is elevated. The EKG shows some widening of the QRS complex (from the hyperkalemia). Toxins and metabolic problems can do this, but sepsis is even less likely now.

Treatment — The tachycardia and dry mouth prompted me to consider that some IV fluids would probably help. The high blood sugar and hyperkalemia (high potassium levels) also made the administration of insulin a good idea, so I started there. I commenced with adding 4 liters of normal saline. With the high potassium, I gave 10 IV units of insulin and an insulin drip to drive potassium from the blood back into the cells. Albuterol (nebulized) also helps to “encourage” the potassium back into the cells. Although I was pretty sure it wasn’t sepsis, I covered my bases by drawing blood cultures and giving a dose of IV antibiotics.

The QRS complex then began to narrow on the monitor. As the fluid was infusing, several measures improved. The heart rate decreased, the breathing slowed, and the patient seemed less groggy. The response to treatment is the clincher for the diagnosis: DKA. I wouldn’t expect fluids and insulin alone to improve the patient’s condition if it were sepsis or toxins. So now the possibility of either of these becomes more remote.

An hour later - A miracle has occurred — the patient is talking! He admits to diabetes, and has not taken any insulin this week. Repeat labs improve on all fronts and he heads off to the ICU. By the time he leaves, I am very confident that I am on track with this patient and his care.

So what are the take-home lessons?

• When you first approach the patient, look at the big picture. Using your eyes alone, you can sometimes get a wealth of information. This patient gave lots of clues just from appearance; he was tachycardic, had dry mouth and skin, and heavy deep breathing, to name a few symptoms.

• If you have in your mind only one possible diagnosis, you aren’t thinking hard enough. Keep your differential diagnosis flexible. Keep getting more information (response to treatment, changing lab values, and reassessments of the patient) and see if those pieces fit with what you think is happening. (Think about an anticholinergic toxidrome.)

• Paramedics did a great job with assessment, stabilization, and treatment of this patient.

• It’s the dehydration and acidosis that cause a patient to succumb to DKA. The elevated sugar doesn’t kill directly, but it does cause the dehydration. Don’t delay the start of IV fluids. It’s pretty hard to hurt a young person with a liter of normal saline quickly infused.

Got an interesting case? Email me a summary, and tell your questions/comments about the ER treatment. I’ll try to write some of the interesting cases!

Robert Donovan, M.D., FACEP, is an emergency physician with a broad background in both pre-hospital and hospital medicine.
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