February 6, 2016

Just Another Nursing Home Transfer

My partner and I went to visit an elderly gent in a nursing home. According to his nurse,* he has baseline type 2 diabetes and dementia, along with some other elderly-related medical problems. He is normally confused, but is slightly more confused over the last few days. The nurse couldn’t really explain how he was more confused than normal; he wasn't her normal patient and she had just began her shift. I asked more specific questions to suss out his baseline mentation. I found out he would normally know his name, but not where he was or any time-related facts. He was not able to perform self-care like bathing or tooth brushing, couldn’t really follow television shows, and he slept a lot. I didn't understand how his mentation had changed, but I wasn't getting closer to finding out.

The patient was recently reported to have some UTI-type symptoms with a little diarrhea over the last week or so. That, along with a possible mental status decline over the last four or five days, resulted in an order for labs to be drawn. His doctor, upon seeing the lab results, asked that the patient be seen at an ED.

I found the patient to be elderly, friendly, and alert to name only. He looked a little dehydrated to me, in that his tongue was dry and he looked like his skin was chapped and flaky. He was a little sleepy, but he woke to voice and interacted in a gentle, confused way.  The patient was neurologically intact, other than his mental status (which I still didn’t understand how it was different than his demented baseline). There were no odors such as ketones on his breath. His blood pressure was 100/50 with a heart rate of 90, but he was a skinny old guy so I found those vitals to be abnormal but not especially concerning. The man certainly wasn’t toxic looking, if that makes sense.  What I mean is that I wasn’t worried about him dying on the way to the hospital or anything. He wasn’t diaphoretic, tachypneic, or comatose. It was a fairly routine transfer from a nursing home to a hospital.

The pertinent parts of his labs, helpfully labeled with L for low and H for high were: 
  • Glucose 964 mg/dL     H (60-110)
  • Potassium 3.2 mEq/L     L (3.5-5.0)
  • Bicarbonate 18.1 mEq/L     L (22-28)
  • Total serum osmolality 382 mOsmol/Kg     H (275-295)
  • Anion gap 11mEq/L       (8-16)
  • β-hydroxybutyrate (serum ketones) normal      (<0.4 mmol/L)

Do you know what is going on? What is your treatment plan?
I think a gummy bear might have less sugar than 964 mg/dL...
Source
The patient is obviously hyperglycemic. But serum ketones are normal, so it isn’t diabetic ketoacidosis.  This is something else – called hyperosmolar hyperglycemic state (HHS). DKA usually affects type 1 diabetics, and HHS is a complication more associated with type 2 diabetes. There are a bunch of other names for it, like hyperosmolar hyperglycemic non-ketotic coma (HHNC) and hyperosmolar non-ketotic coma (HONK – which sounds like a GI issue, not a sugar issue). I like HHS because it is easier to type and remember.

HHS is usually initiated by physiologic stress such as an MI, stroke, or infection. The stressor results in a relative insulin insufficiency, which allows the patient’s blood sugar to rise. The higher blood sugar results in higher serum osmolarity. Osmolarity is the measurement of stuff (solute) dissolved in a liquid (solution); in this case, the amount of salts, sugars, and such dissolved in blood plasma. In short, the ratio of dissolved solutes in the solution tips towards the solute side, rather than the solution (water/plasma) side. The body tries to correct this situation by urinating out the excess sugars.  The increased urination leads to profound dehydration and volume depletion. In contrast to DKA, ketones don’t form because there is some insulin present in the case of HHS patients.

HHS has been reported to occur in about 1 of 500 diabetic patients, so it is much less common than DKA. It is more common in elderly patients, and nursing home patients are at higher risk. HHS is a big deal: mortality is reported at 10-20% of patients, but the risk of death has been reported as higher than that in some studies. 

Treatment is concentrated on three main problems: dehydration, hyperglycemia, and underlying disease treatment.  Dehydration can be profound in HHS patients. Like, nine liters worth of dehydration, profound. When a person is 9 liters down, I can only assume their blood looks like red motor oil. These patients need fluid resuscitation to help correct the dehydration, as well as the hyperosmolarity that is adding to their problems.  
Maybe honey is a better mental picture than motor oil.
Source
The correction of hyperglycemia is through the use of insulin. Before getting aggressive with insulin, however, the patient’s potassium levels must be assessed. Insulin drives potassium into intracellular spaces, resulting in hypokalemia if the initial level of serum potassium is too low. Finally, it is important to remember that HHS is usually caused by a physiologic insult. In the case here, the patient’s infection probably initiated the hyperglycemic event, but other factors like silent MIs, pulmonary embolism, and CVA should be ruled out or treated. 

In the prehospital setting, treatment for HHS is limited to volume replacement. Most systems don’t carry insulin, and if you do make sure to check the potassium first. Keep in mind, though, that “aggressive” volume expansion means something different for other health care providers compared to field medics. I can get a couple of liters into a patient in about fifteen or twenty minutes, if I am really trying.  Aggressive in this case means more along the lines of a liter per hour. Adding your run of normal saline to deranged blood levels of electrolytes and sugars is probably a complicating factor in the absence of hypotension. So consider some fluids, but maybe take it easy.

So why did I bring all this up? I wanted to point out that I don’t recall ever hearing the term HHS, HONK, or HHNC in paramedic school. My endocrine lecture was probably four hours long, and covered a lot more than just DKA and HHS. I am sure we discussed hyperosmolar hyperglycemia, but it was lost in the fire hose of knowledge from which I was trying to drink. The paramedic text I have on my bookshelf behind me has a paragraph on HHS. It says I should treat it with ABCs, oxygenation, ventilatory support, and fluid resuscitation. Duh.

In your career, you will find that your classroom instruction and paramedic texts are inadequate to your knowledge needs. You should discover that. Take the time to look up conditions, medications, treatments, and other medical information as you come across them. The Google-machine or other search engines are incredible tools. UpToDate is a great program and website, but it requires subscription for most services. Medscape is good too, though. Friggin’ Wikipedia can be pretty helpful. Ask physicians at handoff about their thought process and differential diagnoses (after their initial exam, so you don’t interrupt their work) then look up what you don’t know about. Seek out patient follow-up and research the findings that you don’t understand.

What you learned in p-school is not enough. The case here was just a boring nursing home transfer for altered labs and a possible increase in confusion. We run those jobs all the time, and I work for a 911-only service. But look where it took us. Push yourself and your knowledge base farther.



*I use the term “nurse” in its most generic, loosest sense. I never really have any idea if I am dealing with a nurse practitioner, RN, LPN, CNA, or a random member of the public who wandered in off the streets and likes to wear scrubs.

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