What is the mechanism of HHS?

HHS. The basic underlying mechanism of HHS is a relative reduction in effective circulating insulin with a concomitant rise in counterregulatory hormones. Unlike patients with DKA, most patients with HHS do not develop significant ketoacidosis.

What causes hyperosmolar coma?

Diabetic hyperosmolar (hi-pur-oz-MOE-lur) syndrome is a serious condition caused by extremely high blood sugar levels. The condition most commonly occurs in people with type 2 diabetes. It’s often triggered by illness or infection.

What is Hyperosmotic coma?

Hyperosmolar coma is also referred to as hyperosmolar hyperglycemic syndrome (HHS) or nonketotic hyperglycemic syndrome. It is characterized by severe hyperglycemia, hyperosmolality, and dehydration in the absence of significant ketoacidosis. Hyperosmolar coma and diabetic ketoacidosis (DKA) are hyperglycemic crises.

What is the difference between HHS and DKA?

DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis (table 1). Each represents an extreme in the spectrum of hyperglycemia.

What is serum osmolality in HHS?

Serum osmolarity or osmolality Normal serum osmolality ranges from 280 to 290 mOsm/kg. A serum osmolality of 320 mOsm/kg or higher defines HHS. Rarely, serum osmolality may exceed 400 mOsm/kg. In HHS, higher serum osmolality relates to greater impairment of the level of consciousness.

What are the symptoms of hyperosmolar nonketotic coma?

Symptoms

• Blood glucose levels over 600 milligrams per deciliter (mg/dl)
• Frequent urination.
• Extreme thirst.
• Dry mouth.
• Confusion or sleepiness.
• Skin that is warm and dry without sweating.
• Fever (usually over 101 F)
• Weakness or paralysis on one side of the body.

How is hyperosmolar coma treated?

Treatment typically includes:

1. Fluids given through a vein (intravenously) to treat dehydration.
2. Insulin given through a vein (intravenously) to lower your blood sugar levels.
3. Potassium and sometimes sodium phosphate replacement given through a vein (intravenously) to help your cells function correctly.

What happens during diabetic coma?

In a diabetic coma, you are unconscious and unable to respond to your environment. You are either suffering from high blood glucose (hyperglycemia) or low blood glucose (hypoglycemia). You need immediate medical attention if you go into a diabetic coma.

How can you tell the difference between HKA and HHS?

DKA usually evolves rapidly. In HHS, there is little or no ketoacidosis and the serum glucose concentration frequently exceeds 1000 mg/dL. HHS usually evolves over a period of several days. Overlap between DKA and HHS occurs in more than one-third of patients.

Why are there no ketones in HHS?

Serum ketones are not present because the amounts of insulin present in most patients with type 2 diabetes are adequate to suppress ketogenesis.

What is hyperhyperosmolar hyperglycemic non-ketotic coma?

Hyperosmolar hyperglycemic non-ketotic coma is no longer accepted as a diagnostic nomenclature because not all patients with HHS will present with coma even in the presence of significant hyperglycemia and hyperosmolarity. The evaluation of HHS requires a detailed history and physical examination.

What is hyperosmolar hyperglycemic syndrome (HHS)?

This clinical condition was formerly called non-ketotic hyperglycemic coma; hyperosmolar hyperglycemic non-ketotic syndrome, and hyperosmolar non-ketotic coma (HONK).[1] Hyperosmolar hyperglycemic syndrome (HHS) is a clinical condition that arises from a complication of diabetes mellitus. This problem is most commonly seen in type 2 diabetes.

What is the pathophysiology of hyperosmolarity of serum osmolarity?

Higher serum osmolarity is associated with alteration in the level of consciousness and might eventually lead to a coma. The comprehensive metabolic panel allows for the determination of electrolyte derangements seen in HHS.

Does Hyperosmolar therapy reduce intrahepatic cholangiopancreatic cholera (Ich)?

While use of hyperosmolar therapy (HT) has been shown to reduce ICH, its putative pharmacological mechanisms focus on reduction of cerebral edema, yet this would make it potentially ineffective when ICH arises from other etiologies.