What you need to know about diabetic coma

Crucial information about diabetic coma, its causes, symptoms and what can be done. Photo: Freeimages.com

A coma is a state of unconsciousness in which a person does not respond and cannot be awakened.

Although the person is alive, there is minimal brain activity. The eyes will be closed, without any response to sound or pain. There is an inability to communicate, lack of voluntary movements and reduced basic reflexes like coughing and swallowing.

There may be the ability to breathe, although some require assistance from a ventilator.

The Glasgow Coma Scale is used to assess the level of consciousness. It involves an assessment of eye movement, verbal response to a command, and voluntary movements in response to a command. The total score is 15 and most people in a coma have a total score of eight or less.

A coma in diabetics is usually due to very low or very high blood glucose levels. The former is called a hypoglycaemic coma and the latter, a hyperglycaemic coma.

Hypoglycaemic coma

Hypoglycaemia, a condition in which the blood glucose level is lower than normal, is due to an imbalance between glucose supply, glucose utilisation and current insulin levels. The condition is the most common side effect of insulin and sulphonylureas usage in diabetes treatment.

Type 1 diabetics can experience about two episodes of mild hypoglycaemia per week. The annual prevalence of severe hypoglycaemia in unselected populations, has been reported at 30-40% consistently in several large studies.

Severe hypoglycaemia is less common in insulin-treated type 2 diabetes, but it is still a significant clinical problem. Patients with insulin-treated type 2 diabetes are more likely to require hospitalisation for severe hypoglycaemia than those with type 1 diabetes.

A hypoglycaemic coma is more likely to occur if there is inadequate blood glucose monitoring; a large insulin or sulphonylurea overdose; irregular meals; poor appetite; vomiting; increased exercise; impaired liver or renal function; and/or alcohol consumption.

Medicines like warfarin, salicylates, fibrates, sulphonamides (including cotrimoxazole), NSAIDs (non-steroidal anti-inflammatory drugs) and SSRIs (selective serotonin reuptake inhibitors) can also trigger hypoglycaemia.

The symptoms vary, but it has to be considered in any diabetic who is acutely unwell, drowsy, unconscious, unable to co-operate and/or presents with aggressive behaviour or seizures.

Every diabetic with hypoglycaemia should be treated without delay to return the blood glucose levels to normal range.

A quick-acting carbohydrate should be followed up by giving a long-acting carbohydrate, either as a snack or as part of a planned meal.

A blood glucose measurement will be taken to confirm hypoglycaemia. If measurement is difficult, e.g. in someone with a seizure, then treatment should not be delayed.

After acute treatment, a determination will be made as to whether the hypoglycaemia is likely to be prolonged, i.e. as a result of long acting insulin or sulphonylurea, in which case a continuous infusion of dextrose will be necessary to maintain blood glucose levels.

To prevent any hypoglycaemic coma, it is the practice to treat any blood glucose less than 4 mmol/L.

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) occurs when there are very high blood glucose levels (typically above 17 mmol/L) and high ketone levels.


It occurs when there is an inability to use blood glucose because there is insufficient insulin.

Instead, the body breaks down fat as an alternative source of energy. This causes a build-up of potentially harmful by-products called ketones.

The common triggers of DKA include infections like urinary tract infection, gastroenteritis, influenza or pneumonia; missed insulin due to problems with the injector; recent change in the treatment regime; and undiagnosed diabetes, usually type 1.

Other less common triggers include usage of illegal drugs and certain medicines like steroids, as well as heart attacks, strokes and binge drinking.

DKA is common in type 1 diabetics and can occasionally affect type 2 diabetics. It can also occur in those previously not diagnosed with diabetes. It is most common in children and young adults.

The features of DKA include passing large amounts of urine, feeling very thirsty, nausea, vomiting, tiredness, shortness of breath and disorientation, followed by loss of consciousness and coma.

Treatment includes insulin, rehydration with intravenous fluids, and correction of mineral deficits like potassium. Complications of DKA like acute kidney failure, brain oedema and acute respiratory distress are treated accordingly.

Hyperosmolar hyperglycaemic non-ketotic coma

Hyperosmolar hyperglycaemic state (HHS) occurs in poorly con-trolled type 1 or 2 diabetics, but is more common in type 2 diabetics.

It was previously termed hyper-osmolar hyperglycaemic non-ketotic coma (HHNC). The termino-logy was changed because coma is found in less than 20% of patients with HHS.

HHS is less common than DKA.

It is usually triggered by illness, with infection the most common, leading to reduced fluid intake.

As the blood glucose levels increase in HHS, the body tries to get rid of the excess glucose by increased urinary volume. Later, the urine becomes concentrated as dehydration sets in with increased thirst.

Eventually, seizures and HHNC occur, and death results if HHNC is untreated.

HHS may take days or weeks to develop.

The features of HHS include dry, parched mouth; extreme thirst; warm, dry skin that does not sweat and high fever; and later, confu-sion; loss of vision; weakness on one side of the body; seizures and coma.

The blood glucose levels are typically above 33 mmol/L.

The treatment of HHS include vigorous rehydration; maintenance of electrolyte balance; correction of hyperglycaemia; treating any underlying condition; and supporting cardio-respiratory, kidney and central nervous system function.

Prevention measures

The features of HHS and DKA overlap in as many as one third of cases and are observed simulta-neously.

This suggests that these two states of uncontrolled diabetes differ only with respect to the magnitude of dehydration and the severity of acidosis.

The following measures can prevent hypoglycaemic and hyperglycaemic diabetic comas:

• Ensure diabetes is well controlled

• Keep appointments with the doctor

• Be aware of the symptoms of high and low blood glucose

• Check blood glucose levels more frequently when ill

• Continue taking insulin and sulphonylureas when ill

• Keep oneself well hydrated

• Consume alcohol in modera-tion, or better still, avoid it altoge-ther, especially after strenuous exercise

• Beware of hypoglycaemia at night following exercise, if taking insulin or sulfonylureas

• Check for ketones if blood glucose levels are high in type 1 diabetes. In general, a blood glucose of 11 mmol/L or more is indicative of an increased risk of DKA.

The take home message is prevention is better than cure.

Dr Milton Lum is a member of the board of Medical Defence Malaysia. The views expressed do not represent that of organisations that the writer is associated with. The information provided is for educational and communication purposes only and it should not be construed as personal medical advice. Information published in this article is not intended to replace, supplant or augment a consultation with a health professional regarding the reader’s own medical care. The Star disclaims all responsibility for any losses, damage to property or personal injury suffered directly or indirectly from reliance on such information.

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