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
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?
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| 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.
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| 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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