Hyperosmolar hyperglycemic state: Clinical sciences

Hyperosmolar hyperglycemic state, or HHS for short, is a life-threatening complication of type 2 diabetes mellitus. It is usually triggered by a precipitating factor, such as illness or infection, that eventually leads to relative insulin deficiency, hyperglycemia, and elevated serum osmolality.

Keep in mind that there’s a higher risk of HHS in older individuals, especially those with impaired cognitive function or thirst perception, as well as those who do not adhere to their treatment regimen for diabetes. The diagnosis of HHS requires lab workup that demonstrates an elevated blood glucose and serum osmolality, as well as the absence of metabolic acidosis and ketonuria.

Now, if you suspect HHS, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. HHS generally presents as unstable, so stabilize the airway, breathing, and circulation. Next, obtain IV access and give 1-liter bolus of isotonic IV fluid. Next, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, and provide supplemental oxygen, if needed.

Once you stabilize the patient, obtain a focused history and physical exam. Your patient typically reports polyuria, polydipsia, weakness, lethargy, or even seizures. These are commonly associated with a recent precipitating illness or infection. Additionally, there might be a known history of diabetes with inadequate glycemic control or recent disruption in therapy.

On the other hand, a physical exam might reveal signs of severe dehydration, such as dry mucous membranes, tachycardia, and hypotension. In severe cases, you might even notice somnolence and focal neurologic deficits, such as visual disturbance.

Based on these findings, suspect HHS and order labs, including an ABG or VBG, a serum osmolality, a CMP, and a urinalysis. Next, review the lab results and assess diagnostic criteria for HHS, which include blood glucose above 600 mg/dL; serum osmolality over 320 mOsm/kg; the absence of metabolic acidosis; and minimal or no ketonuria.

If diagnostic criteria for HHS are not met, you should consider alternative diagnoses. On the other hand, if the lab results show that HHS criteria are met, you can diagnose HHS and begin insulin treatment.

Here’s a clinical pearl! HHS can present with signs and symptoms that are similar to diabetic ketoacidosis, or DKA for short. Unlike HHS though, in DKA, the distinguishing feature is a ketoacidosis, with a pH under 7.3 and a serum bicarbonate below 15. Also, the serum glucose in DKA is usually less than 600 mg/dL. Another condition that may masquerade as HHS is diabetes insipidus. Individuals with diabetes insipidus can also present with extreme thirst, polyuria, lethargy, and increased serum osmolality, but unlike in HHS, hyperglycemia is not a feature of this condition.

Ok, now that we’ve diagnosed HHS, let’s turn our attention to management. Start with immediate IV fluid resuscitation, as well as a bolus of IV insulin, dosed at 0.1 unit per kilogram, followed by a constant IV insulin infusion at 0.1 units per kilogram per hour. At the same time, pay attention to the serum potassium level, because insulin and fluid resuscitation can lower serum potassium levels. If the serum potassium is above reference range, no potassium replacement is needed. On the other hand, if the serum potassium is below reference range or even within reference range, add potassium to the IV fluids. In fact, if the potassium is below the reference range, it's actually necessary to replace potassium before even starting insulin!

Here’s a high-yield fact to keep in mind! As soon as you give insulin, it will shift potassium from blood right into the cells, dangerously decreasing its blood levels. So a modestly low potassium of 3 could quickly reach a lethal level of 2.5 if you start the insulin drip before appropriately replacing the potassium.