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How hyperglycemic are you? Clinical approach to the Hyperglycemic Hyperosmolar Patient (HHS) – Part 2 | VETgirl Veterinary Continuing Education Podcasts

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In this VETgirl online veterinary continuing education podcast, VETgirl Co-Founder Dr. Garret Pachtinger, DACVECC reviews part 2 of treatment of the endocrine emergency in dogs and cats: hyperglycemic hyperosmolar syndrome (HHS). In the previous VETgirl podcast on HHS, we reviewed the subtle differences of patients with HHS as compared to diabetic ketoacidosis (DKA), HHS criteria, and common clinical signs.

In this Part 2 VETgirl podcast, we will review more specific diagnostics, treatment goals, and the prognosis for HHS.

If you haven’t listened to Part 1, check that out first. But in brief summary, the criteria for HHS that we mentioned in the previous podcast include:
– Glucose > 600 mg/dL
– Serum Osmo ≥ 320 mmol/L
– Profound dehydration
– pH > 7.3
– Bicarb > 15 mEq/L
– Absent to small ketonuria/ketonemia
– Altered level of consciousness.

Let’s dive a little deeper into diagnostics to consider and common abnormalities for HHS patients.

Routine laboratory findings including evaluation of a complete blood count, serum biochemistry, and urinalysis include:
– Severe hyperglycemia (BG > 600 mg/dL or > 33.3 mmol/L)
– Glucosuria
– Trace or absent ketones
– Mild to no metabolic acidosis.
– Elevated packed cell volume (PCV) likely as a result of dehydration.
– Azotemia and hyperphosphatemia (either as a result of a secondary disease process, dehydration, and/or decreased GFR)
– Electrolyte abnormalities including hypokalemia as well as potential hyponatremia (as compared to possible pseudohyponatremia as a result of the severe hyperglycemia).

An important note and diagnostic to evaluate in these patients is to calculate their serum osmolality. Osmotically active particles such as sodium, glucose, and blood urea nitrogen (BUN) can dramatically affect the serum osmolarity. A normal plasma osmolality is ~ 290 mmol/L. A patient is considered hyperosmolar when plasma osmolality is > 310 mmol/L. Notably, we discussed earlier that HHS patients often have an osmolality > 320 mmol/kg. This hyperosmolality results in dehydration of neurons in the brain which can result in these various neurologic symptoms. Neurologic signs are more likely when the patient’s serum osmolality > 340 mmol/L.

Our VETgirl members can find this equation written out on this podcast page on our website, but for this listening, here is how you calculate serum osmolality

The formula is 2(Na+K) + Glu/18 + BUN/2.8

As we mentioned earlier, a high plasma osmolality causes fluid to shift from intracellular spaces to the extracellular space in effort to maintain equilibrium. When this happens in the brain, the result is dehydration of the neurons. If this is chronic, the body responds to protect the brain by making idiogenic osmoles to maintain cerebral water balance. , similar to what happens in hypernatremic conditions. This is important to remember when starting treatment on these patients. We do not want to either lower or raise sodium too quickly in chronic conditions!

Of course additional diagnostics such as imaging studies will be needed in looking for primary or secondary disease processes, similar to the way you would further evaluate a DKA patient.

Let’s dive into treatment

HHS is complex disease process and we have to be meticulous when developing a treatment plan for a patient with HHS. Common treatment goals include the use of:

1) Fluid therapy – to include fluid resuscitation as these patients typically have large volume deficits. Remember, when creating a treatment plan we focus on 4 pillars of fluid therapy. Shock boluses followed by maintenance, dehydration, and ongoing losses once out of shock. Remember, in these cases sodium should not be changed rapidly. Idiogenic molecules cannot dissipate rapidly, so rapid changes in sodium and therefore plasma osmolality can lead to a worsening of the patient’s neurologic signs. Osmolality must be decreased very slowly at a rate no more than 10–15 mOsm/day.

Sodium levels are not the only factor related to osmolarity. In thinking about the equation discussed earlier, glucose levels must be lowered slower than those of a DKA patient.

Fluid therapy may also be used for electrolyte correction.

2) Other therapies may include:
– Antiemetics
– Antibiotic therapy
– And other ancillary supportive care.

Ultimately, one of the most complicated questions and what we need to educate families on is the prognosis of HHS. The mortality rate for HHS is higher than that of DKA, with human mortality rates varying from 10–50%. My clinical experience is that there is a 50% survival rates for these patients, and unfortunately a high cost for diagnosis, treatment, and both short and long term follow-up.

  1. Mahdi Haghighat says:

    Hi Garret,
    Thank you for the wonderful HHS CE podcast.
    I was wondering if you can give us some hints about insulin therapy in this cases as well.
    Is there any formula or guideline for treating these cases as it is with DKA(Insulin & Dextrose CRI chart)?

    Thank you in advance,

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