Diabetic coma

Classification according to ICD-10
E10.0-	Primarily insulin-dependent diabetes mellitus [type 1 diabetes]: With coma
E11.0-	Not primarily insulin-dependent diabetes mellitus [type 2 diabetes]: With coma
E12.0-	Diabetes mellitus in connection with malnutrition or malnutrition [malnutrition]: With coma
E13.0-	Other specified diabetes mellitus: With coma
E14.0-	Unspecified diabetes mellitus: With coma
ICD-10 online (WHO version 2019)

The diabetic coma (Latin coma diabeticum ) or hyperglycemic coma is a severe metabolic imbalance triggered by an absolute or relative insulin deficiency with impaired consciousness and even unconsciousness ( coma ). However, according to neurological definition, only about 10% of patients are really unconscious. A coma is a life-threatening situation and requires immediate hospital treatment. In about 25% of the cases, it is a newly discovered diabetes mellitus .

Trigger mechanisms of the diabetic coma

• Lack of insulin supply: In addition to the first manifestation of diabetes mellitus, a failure to inject insulin for several hours or days can be the cause. Oral drug therapy for diabetes can also no longer be sufficient and lead to a diabetic coma.
• Insufficient insulin supply: This can occur with poorly controlled diabetes mellitus as well as with continued errors in the operation of the syringes, pens or insulin pumps.
• Increased insulin requirement: In the event of an unusually high calorie intake, sudden lack of exercise or prolonged stressful situations (e.g. infection, accident, serious illness, surgery), the previous insulin dose is no longer sufficient.

Forms of diabetic coma

There are two forms of diabetic coma: diabetic ketoacidosis (ketoacidotic coma) and hyperosmolar hyperglycemic syndrome (hyperosmolar coma).

Ketoacidotic coma

The ketoacidotic coma is typical of type 1 diabetes, i.e. it occurs when there is an absolute lack of insulin. Since the pancreas no longer produces insulin and the cells cannot absorb sugar from the blood via GLUT-4 transporters, the body tries to gain energy by breaking down fats and proteins. "Acid" metabolic products arise, e.g. B. ketone bodies .
The blood sugar is between 16.65 and 38.85 mmol / l (300–700 mg / dl). The increased blood sugar level causes increased urine excretion ( polyuria ), since the glucose in the tubule system of the kidney cannot be completely reabsorbed, which leads to osmotic diuresis . In addition, there is acidosis ( acidosis ) due to the derailed metabolism. The body tries to compensate for this by exhaling more carbon dioxide . Typical for this is frequent, regular, deep breathing ( kissing mouth breathing ) with an acetone odor. The polyuria leads to dehydration , which can lead to prerenal kidney failure , the blood salts ( electrolytes ) increase, especially the potassium is greatly increased. Massive abdominal pain (hard stomach: pseudoperitonitis ) is typical , and cardiac arrhythmias can also occur.

Hyperosmolar coma

The hyperosmolar coma is typical of type 2 diabetes, i.e. it occurs when there is a relative lack of insulin. The body's own insulin is still produced, which is sufficient to inhibit the excessive breakdown of fat and protein.
The problem here is the massively increased blood sugar levels (BG> 33.3 mmol / l [600–1000 mg / dl]). The osmolarity of the blood increases due to the high blood sugar . Here, too, the polyuria leads to dehydration, which can lead to prerenal kidney failure, the blood salts (electrolytes) increase, in particular the potassium is greatly increased. Desiccosis in particular leads to increasing apathy and even coma.

Symptoms

Smell of acetone in the breath (smell of rotten apple, also formerly contained in nail polish or nail polish remover) in ketoacidotic metabolic disorders, thirst and excessive drinking ( polydipsia ), frequent urination (polyuria), tiredness, nausea, vomiting, abdominal pain, hypotension, weakened muscle reflexes may precede the development of a diabetic coma as a warning sign.

therapy

Apart from an emergency call and using the stable side position , the first aider has no options for intervention after the coma has occurred.

The most important primary measure is the intravenous supply of fluids ( electrolyte solution ) already by the rescue service. The administration of insulin is reserved for inpatient therapy, since insulin, in addition to its blood sugar-lowering effect, also promotes the absorption of potassium into the cells. Since the plasma potassium cannot be controlled preclinically, there is a risk of hypokalaemia , which increases the stimulus threshold for the excitability of cells. This can be particularly noticeable in the heart as malignant arrhythmias. The gradual normalization of the metabolic values ​​takes place under close laboratory control of the kidney values, the electrolytes, the pH value and the blood sugar.

After a normal metabolism has been achieved, the diabetes mellitus is reset, depending on the type of diabetes (type 1, type 2) and the cause of the metabolic imbalance.

literature

• J. Hensen, T. Thomas, J. Müller-Ziehm: Diabetic ketoacidosis and non-ketoacidotic hyperosmolar diabetic coma . Drug Therapy 2006; 24: 432-43

This article is about a health issue. It is not used for self-diagnosis and does not replace a diagnosis by a doctor. Please note the information on health issues !