What is the pathophysiological process contributing to hyperglycemia in the patient presenting with HHS?

In the context of hyperglycemia associated with Hyperglycemic Hyperosmolar State (HHS), the key pathophysiological process is indeed the alteration in insulin regulation, but it’s important to understand the interplay rather than pointing to a single factor as the singular cause of hyperglycemia.

The primary contributors to hyperglycemia in HHS include significant insulin resistance and decreased effective insulin action, compounded by a relative deficiency in insulin production due to the extreme stress of the state.

In situations of severe illness or stress, there is typically an increase in counter-regulatory hormones, including glucagon and cortisol. Cortisol, in particular, plays a vital role in glucose metabolism by increasing gluconeogenesis and reducing the effectiveness of insulin, further contributing to sustained high blood glucose levels.

Therefore, increased cortisol release contributes to the hyperglycemic state; it facilitates an elevated glucose output from the liver while simultaneously inhibiting glucose uptake in peripheral tissues. As a result, this leads to a state of hyperglycemia which is characteristic of HHS. Insulin resistance also plays a critical role here, but the direct contribution of cortisol in the context of severe stress helps to underscore why this hormone's elevated levels are pivotal in driving the glucose imbalance in patients