Non-Ketotic Hyperosmolar Hyperglycaemia PDF

non-ketotic hyperosmolar hyperglycaemia Introduction Hyperosmolar hyperglycemic state (HHS), also known as hyperosmolar non-ketotic state (HONK), is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. Signs and symp...

non-ketotic hyperosmolar hyperglycaemia Introduction Hyperosmolar hyperglycemic state (HHS), also known as hyperosmolar non-ketotic state (HONK), is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. Signs and symptoms Symptoms of HHS include:Altered level of consciousness Neurologic signs including: blurred vision, headaches, focal seizures, myoclonic jerking, reversible paralysis[ 6]Motor abnormalities including flaccidity, depressed reflexes, tremors or fasciculationsHyperviscosity and increased risk of blood clot formationDehydration  Weight loss 6]Nausea, vomiting, and abdominal pain Weakness 6]Low blood pressure with standing Cause The main risk factor is a history of diabetes mellitus type 2. Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1. Triggers include infections, stroke, trauma, certain medications, and heart attacks.Other risk factors:Lack of sufficient insulin (but enough to prevent ketosis)Poor kidney functionPoor fluid intake (dehydration)Older age (50–70 years)Certain medical conditions (cerebral vascular injury, myocardial infarction, sepsis)Certain medications (glucocorticoids, beta-blockers, thiazide diuretics, calcium channel blockers, and phenytoin) Diagnosis Plasma glucose level >30 mmol/L (>600 mg/dL) Serum osmolality >320 mOsm/kg Profound dehydration, up to an average of 9L (and therefore substantial thirst (polydipsia)) Serum pH >7.30 Bicarbonate >15 mEq/L  Small ketonuria (~+ on dipstick) and absent- to-low ketonemia ( 30 mg/dL (increased) Creatinine > 1.5 mg/dL (increased) if MRI is performed, it may show cortical restricted diffusion with unusual characteristics of reversible T2 hypointensity in the subcortical white matter Differential Diagnosis The major differential diagnosis is diabetic ketoacidosis (DKA). In contrast to DKA, serum glucose levels in HHS are extremely high, usually greater than 40-50 mmol/L (600 mg/dL).  DKA often has serum glucose level greater than 300 mg/dL (HHS is >600 mg/dL). DKA usually occurs in type 1 diabetics whereas HHS is more common in type 2 diabetics. DKA is characterized by a rapid onset, and HHS occurs gradually over a few days. DKA also is characterized by ketosis due to the breakdown of fat for energy.Both DKA and HHS may show symptoms of dehydration, increased thirst, increased urination, increased hunger, weight loss, nausea, vomiting, abdominal pain, blurred vision, headaches, weakness, and low blood pressure with standing Management Intravenous fluids Treatment of HHS begins with reestablishing tissue perfusion using intravenous fluids. People with HHS can be dehydrated by 8 to 12 liters. Attempts to correct this usually take place over 24 hours with initial rates of normal saline often in the range of 1 L/h for the first few hours or until the condition stabilizes. Electrolyte replacement Potassium replacement is often required as the metabolic problems are corrected. It is generally replaced at a rate 10 mEq per hour as long as there is adequate urinary output Insulin Insulin is given to reduce blood glucose concentration; however, as it also causes the movement of potassium into cells, serum potassium levels must be sufficiently high or dangerously low blood potassium levels may result. Once potassium levels have been verified to be greater than 3.3 mEq/L, then an insulin infusion of 0.1 units/kg/hr is started. The goal for resolution is a blood glucose of less than 200 mg/dL Thanks