Podcasts

Join Now

How hyperglycemic are you? Clinical approach to the Hyperglycemic Hyperosmolar Patient (HHS) – Part 1 | VETgirl Veterinary Continuing Education Podcasts

Need Help?

In this VETgirl online veterinary continuing education podcast, VETgirl Co-Founder Dr. Garret Pachtinger, DACVECC reviews hyperglycemic hyperosmolar syndrome (HHS) in dogs and cats.

While many of us are familiar with diabetic ketoacidosis (DKA) as a life threatening form and complication of diabetes, one of the ‘zebras’ that we see more often than a zebra at the zoo is known as hyperglycemic hyperosmolar syndrome (HHS). HHS was formerly known as hyperglycemic hyperosmolar nonketotic coma or syndrome (HHNC, HHNS, or HONK), nonketotic hyperosmolar syndrome (NKHS), or a variety of other acronyms.

HHS is seen in patients with diabetes mellitus with profound hyperglycemia (BG > 600 mg/dL or > 33.3 mmol/L), along with hyperosmolarity (> 320 mOsm/kg), extreme dehydration, CNS depression, with absent-to-low ketonemia and lack of significant metabolic acidosis (pH > 7.3).

Criteria for HHS includes:
– Glucose > 600 mg/dL
– Serum Osmo ≥ 320 mmol/L
– Profound dehydration
– pH > 7.3
– Bicarb > 15 mEq/L
– Small to absent ketonuria / ketonemia
– Altered consciousness

The approach to understanding and diagnosing a patient with HHS is similar to that of diagnosing a DKA. In health, insulin is produced from beta cells in the islets of Langerhans, found primarily in the pancreas. Both DKA and HHS have either a relative or absolute deficiency of insulin in combination with an overabundance of counterregulatory hormones. In these patients, these cells are not producing enough or any insulin which results in elevated levels of counterregulatory hormones such as glucagon, catecholamines, and cortisol. All of these hormones promote glycogenolysis and gluconeogenesis in the liver. While the liver is stimulated to produce glucose, cells are unable to utilize this glucose due to lack of insulin and high catecholamine concentrations, which also reduce uptake of glucose by peripheral tissues. This combination of increased production of glucose and decreased use or uptake of the glucose results in hyperglycemia.

If we compare DKA and HHS, in the DKA patient the combination of absolute insulin deficiency and elevated catecholamines, cortisol, and growth hormones activates the release of hormone-sensitive lipase, the subsequent breakdown of triglycerides, leading to the release of free fatty acids from adipose tissue and ultimately ketogenesis. In the HHS patient ketogenesis does not occur. It is thought that HHS patients have some circulating insulin and only a relative insulin deficiency. This presence of small amounts of insulin prevents development of ketosis by preventing lipolysis. So, HHS patients have a relative lack of insulin, persistent hyperglycemia, an osmotic diuresis and counterregulatory hormone release without ketonemia.

What are the clinical Signs of HHS? Common signs of illness in HHS patients include dehydration, lethargy, mental depression (including profound depression or even coma), abdominal pain, anorexia, and vomiting. These patients may have additional neurological signs due to the hyperosmolarity including abnormal pupillary light response, circling, pacing, and tremor/seizure behavior.

Tune in next week for Part 2 of HHS, where we review the diagnostic and treatment approach – and prognosis – in HHS patients!

Only VETgirl members can leave comments. Sign In or Join VETgirl now!