Diabetic hyperosmolar coma

The article was professionally consulted by a General Internal Medicine Doctor - Department of Examination & Internal Medicine - Vinmec Nha Trang International General Hospital.

Hyperosmolar coma occurs when a patient's glycemic index is elevated with high osmolality. Acidosis in coma is not significantly increased osmotic pressure, pH is often greater than 7.3, ketosis does not occur or is only minimal.

Symptoms of hyperosmolar coma in patients with diabetes:
Consciousness disturbances with varying degrees from lethargy to deep coma.
Patient has signs of severe dehydration such as: dry skin, slow loss of skin folds, rapid pulse, low blood pressure...
Symptoms of other triggers such as infection, vascular accident Brain ...

Glycemic index > 40mmol/l Plasma osmolality > 320 mOsm/l. Arterial blood gases: pH > 7.3, bicarbonate > 15mmol/l No or very little ketonuria. Hypernatremia > 145 mmol/l but may still be normal.

Ketoacidosis is characterized by elevated blood glucose levels greater than 300 mg/dL, blood pH < 7.3, alkaline reserves less than 15 mEq/l, blood ketones and strongly positive urine ketones Increased osmolarity occurs when glucose Blood elevation > 400 mg/dL in most cases, blood osmolality > 320 mOsm/Kg water but negligible acidosis, pH > 7.3, no or little ketosis. Statistically, ketoacidosis occurs 6-8 times more often than coma with hyperosmolarity. Ketoacidosis is common in type 1 diabetes while hyperosmolarity mainly occurs in type 2 diabetes, especially in women over 50 years of age. Hyperosmolar coma has a higher mortality rate than diabetic ketoacidosis.

Hyperosmolar coma and ketoacidosis both have a common background of absolute or relatively severe insulin deficiency, accompanied by an increase in insulin resistance hormones. In the absence of insulin, tissue glucose uptake is reduced and tissue glucose utilization is also reduced. Without insulin, the liver will increase the production of glucose into the blood.
When the deficiency is severe, adipose tissue will be lysed, triglycerides hydrolyze into glycerol and fatty acids, glycerol will generate sugar, a small part of fatty acids is used for energy, most of which is taken to the liver. In the liver, fatty acids are taken into the mitochondria and oxidized by beta to ketone bodies.
Decreased glucose uptake in muscle tissue and increased glucose production from the liver will increase blood sugar, if blood sugar is greater than 200 mg/dL, sugar will appear in the urine, sugar is a substance with high osmotic pressure causing high blood sugar. osmotic polyuria, the patient loses water and electrolytes, especially potassium and sodium.
However, in hyperosmolar coma, there is usually no or very little ketosis, and this mechanism is not completely understood. It is assumed that patients with type 2 diabetes have only a relative insulin deficiency, and levels of insulin resistance hormones and free fatty acids are also often lower in ketoacidosis. In addition, the insulin/glucagon ratio in hyperosmolar conditions does not decrease to a level that favors the formation of ketone bodies.

Principles of management First aid ABC Place a large intravenous line, place a central venous catheter. Monitor capillary blood sugar every 3 hours, use insulin to control blood sugar. Monitor electrolytes every 6 hours until the patient is stable. Diagnosis and treatment of favorable causes of increased osmotic pressure (pneumonia, urinary tract infections...).

Management of fluid resuscitation Start infusion of 1000ml of 0.9% NaCl over 1 hour, estimated water loss is about 8-10 liters If there is severe dehydration causing hypotension: administer 0.9% NaCl 1000ml/hour until systolic blood pressure is over 90mmHg If Na concentration is normal or increased: Infuse 0.45% NaCl 250-500ml/hour depending on dehydration, when blood glucose is 16.5mmol/l add 5% glucose plus 0.45% NaCl at 150-250ml/ hour If Na concentration decreases: infusion of 0.9% NaCl 250-500ml/hour depending on dehydration status, when blood glucose is 16.5 mmol/l, add 5% glucose with 0.45% NaCl at the rate of 150-250ml/hour. Insulin administration Intravenous insulin 0.1 units/kg followed by continuous intravenous infusion of 0.1 units/kg/hour If blood glucose does not decrease by 3.0 mmol/l within the first hour, the insulin dose can be doubled. When blood glucose reaches 16.5 mmol/l, reduce insulin dose to 0.02-0.05 units/kg/hour, ensuring blood glucose 11-16.5 mmol/l until patient regains consciousness. Potassium ion compensation If the patient's renal function is normal (urine output > 50 ml/hour) If serum potassium is < 3.5 mmol/l, administer insulin and intravenous infusion of 20-30 mmol potassium/hour until serum potassium levels are reached. > 3.5mmol/l If the initial serum potassium is 3.5-5.3 mmol/l, add potassium 20-30mmol/l of the intravenous fluid to ensure that the serum potassium level is maintained between 4-5mmol/l. If baseline serum potassium >5.3 mmol/l, without potassium replacement, check serum potassium every 2 hours. When the patient is fine, can eat, switch to subcutaneous insulin, continue IV insulin 1-2 hours after subcutaneous insulin injection to ensure adequate insulin concentration in the blood. Manage causes of decompensation (favorable factors) Antibiotics are indicated when there is evidence of infection. Use anticoagulants to prevent thrombosis. Currently, Vinmec International General Hospital is providing a diabetes screening package to help patients detect the disease early and improve treatment efficiency.
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