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Classification according to ICD-10
E14.6 Unspecified diabetes mellitus with other specified complications
E15 Hypoglycemic coma, nondiabetic
E16.0 Drug-induced hypoglycemia without coma
E16.1 Other hypoglycaemia
E16.2 Hypoglycaemia, unspecified
P70.0 Syndrome of a mother's child with gestational diabetes mellitus
P70.1 Syndrome of the child of a diabetic mother
P70.3 Iatrogenic hypoglycemia in the newborn
P70.4 Other neonatal hypoglycaemia
ICD-10 online (WHO version 2019)

Hypoglycemia , also hypoglycemia written ( coll .: hypoglycemia ) referred to in the medicine an abnormally low blood sugar levels (too low a concentration of glucose in the blood ).

Although blood sugar limit values ​​are difficult to set due to interindividual differences, in the current specialist literature, blood sugar values ​​below 50–60 mg / dl (2.77–3.3 mmol / l ) indicate hypoglycaemia even without other symptoms, and even below 70 if there are recognizable symptoms mg / dl (3.9 mmol / l).

A distinction is made between hypoglycemia without symptoms ("asymptomatic hypoglycemia") and one with symptoms ("symptomatic hypoglycemia"). With the latter, a distinction is made between two degrees of severity, on the one hand whether the person concerned can still help himself or whether he is dependent on outside help. Classic symptoms are, depending on the duration and severity of the condition, for example sweating and clouding of consciousness through delirium to coma ( hypoglycemic coma , colloquially known as sugar shock ). Untreated, severe and persistent hypoglycemia can be fatal. It must not be confused with the diabetic coma (coma diabeticum) , a severe metabolic derailment with excess sugar (hyperglycemia) .

Certain cells in the human body, such as brain cells, are dependent on a continuous supply of energy in the form of glucose. In hypoglycemia, the sugar content of the blood drops so much that the cells' ability to function is impaired. Therefore, in metabolically healthy people, the first compensation mechanisms appear at levels below about 60 mg / dl, the aim of which is to increase the blood sugar level again. Thanks to these compensation mechanisms, there are no threatening hypoglycemias, even during long periods of hunger. The cause of hypoglycemia is usually a relative excess of the blood sugar-lowering hormone insulin in the blood, or an overdose of blood-sugar-lowering drugs such as certain anti-diabetic drugs , whereby the physiological compensation mechanisms are overwhelmed. Such hyperinsulinemia is usually caused by an overdose of an insulin injection as part of the treatment of diabetes ( diabetes mellitus ). In very rare cases, insulin-producing tumors ( insulinomas ) can also be the cause.

The therapy of hypoglycaemia consists of the oral administration of glucose. In a medical emergency or when the patient cannot swallow, glucose must be administered intravenously. In emergency medicine, glucagon can also be administered intramuscularly or subcutaneously to increase blood sugar . In the long term, it is advisable to stabilize the blood sugar level by improving insulin therapy or eliminating other causes (e.g. removing an insulinoma ).


A common definition of hypoglycemia from 1983 describes a blood sugar level below 40 mg / dl without symptoms or 50 mg / dl with symptoms. The blood sugar level at which symptoms occur varies from person to person. The rapid lowering of an elevated blood sugar level also favors their occurrence. Therefore, in more modern definitions, hypoglycemia is further classified clinically into four levels from mild to moderate to severe and severe with medical intervention.


Hypoglycaemia is of quantitative importance, especially in diabetics who are treated with medication. It is estimated that, of the type 2 diabetic patients treated with sulfonylureas in the UK, more than 5,000 patients per year experience severe emergency hypoglycemia. The cost of hospitalization for severe hypoglycemia in the UK is estimated at £ 1,000 per case.

Repeated severe hypoglycaemia also appears to favor the development of dementia . In the case of severe hypoglycemia, the dementia rate increased in the observed patients by 26 percent after evaluating the medical records, in two episodes by 80 percent and in three the dementia rate almost doubled.

Pediatric hypoglycaemia after delivery is the quantitatively most significant complication following a maternal diabetic metabolic condition during pregnancy .


The cause of low fasting blood sugar is the increased secretion of insulin from the pancreas, including the insulinoma and generally hyperinsulinism , severe liver diseases in which gluconeogenesis or the release of glucose into the blood ( glycogen storage disease ) is restricted, uremia , which is associated with insufficiency of adrenal or pituitary raising your blood sugar associated reduction hormones that sugar excretion via the kidneys and tumors such as hepatocellular carcinoma . The excretion of insulin-like peptides in the context of paraneoplasia and glycogenoses can also be responsible for this. Low fasting blood sugar can also occur in newborns whose mothers are diabetic or in children with congenital hyperplasia of the islet cells of the pancreas .

Postprandial hypoglycaemia is found in gastric emptying disorders , in the initial stage of diabetes mellitus, after gastric resections , as a result of hereditary diseases such as fructose intolerance and reactive after short-term intake of high amounts of sugar or vegetative lability with increased vagotonia .

Typical external causes of hypoglycaemia are an excessive dose of insulin or sulphonylureas and excessive alcohol consumption without food. Vigorous physical exertion can also lead to hypoglycaemia.


Various mechanisms are involved in regulating the blood sugar level in healthy people. So it lowers the pancreas secreted insulin by stimulating the uptake of glucose ( glucose increases) in fat and muscle cells. At the same time, however, the human body also has mechanisms at its disposal to increase a lowered blood sugar level. One of the main ones is glucagon , which stimulates gluconeogenesis . Hypoglycemia occurs when the body's actions to increase blood sugar cannot compensate for those that lower blood sugar. In the brain , which relies on glucose as the main energy supplier , the glucose concentration is normally 4 to 6 mM (5 mM corresponds to 90 mg / dL), but drops to 2 to 3 mM during fasting . Below 1 mM, confusion occurs, and below 1 mM, coma occurs.

This can occur not only in diabetics who have been given too much insulin , for example , but also in metabolically healthy people. In reactive hypoglycemia, a short-term, high-dose supply of sugar stimulates the insulin release so intensively that the compensation mechanisms are overwhelmed. An analogous mechanism is also the basis of dumping hypoglycemia as a result of a disturbed reservoir function of the stomach ( dumping syndrome ) after surgical interventions on the gastrointestinal tract .

Hypoglycemia in diabetes mellitus

The treatment of diabetes mellitus (diabetes) can lead to hypoglycaemia. The administration of insulin itself can lead to hypoglycaemia in the event of an overdose, insufficient carbohydrate intake, uncalculated exercise or accidental intramuscular injection. If type 2 diabetics are treated with insulin, the frequency of severe hypoglycaemia - depending on the stage of insulin resistance - is close to that of type 1 diabetics. The duration of insulin treatment (and thus the duration of the illness) is the main predictor of hypoglycaemia in type 2 diabetes. An incorrect perception of hypoglycemia typically occurs in type 1 diabetics who have had a long illness. Two mechanisms play a role:

  • In the course of the disease, in addition to the insulin deficiency, hormonal opponents such as B. Glucagon .
  • Then when the diabetic, e.g. B. for fear of consequential damage, his blood sugar always keeps near-hypoglycemic, he trains his body downright for low blood sugar values. Then it can happen that adrenergic symptoms (caused by adrenaline) are no longer noticed and unconsciousness occurs relatively suddenly at blood sugar levels of approx. 27 mg / dl.

The active ingredients from the group of sulfonylureas (especially glibenclamide and glimepiride ) can also lead to hypoglycaemia. Here, too, the higher the number of hypoglycaemia experienced in a short period of time, the lower the perception threshold for them. This makes unnoticed but life-threatening hypoglycaemia possible.

The precise determination of the frequency of hypoglycaemia in type 2 diabetics is underestimated since most patients are middle to elderly. In the elderly, symptoms are usually associated with cognitive disorders. The main clinical problem, however, is that these hypoglycaemia can often last for hours to days.

Other causes

Even people without diabetes mellitus can get hypoglycaemia: with vigorous physical activity (e.g. through sport; see hunger rest ), high stress levels and meals that induce very strong insulin secretions (high glycemic index ). In terms of differential diagnosis, one should also think of malabsorption (i.e. insufficient intake) of carbohydrates and nutrients. This can be related in particular to gluten intolerance ( celiac disease ) (which has sometimes remained undetected for years ), in which the mucous membrane of the small intestine is so severely affected as part of an autoimmune reaction through the absorption of gluten ( mainly contained in wheat, barley, spelled and rye and in many ready-made meals and meat products) What is damaged is that carbohydrates and nutrients cannot be used to a sufficient extent ( see also postprandial hypoglycaemia, formerly also known as functional or reactive hypoglycaemia).

Drugs such as salicylic acid and its derivatives can cause hypoglycaemia by disrupting the body's mobilization of sugar from the liver. The drug pentamidine used against leishmaniasis has a direct toxic effect on the insulin-producing cells and, by destroying them, can trigger the body's own insulin release with hypoglycaemia. Quinines and sulfonamide antibiotics also promote insulin release. Similarly, quinolone antibiotics and rarely used today beta-blocker propranolol associated with hypoglycemia in combination. Beta blockers can mask the warning signs of hypoglycaemia by acting on peripheral beta receptors .

In very rare cases, adrenal insufficiency due to a failure of the adrenal cortex hormone cortisol , a thyroid hormone disorder or a disease of the pituitary gland can lead to hypoglycaemia. An insulinoma , an insulin-producing tumor, is also rare .

Hypoglycaemia can develop after consumption of alcohol , as alcohol inhibits gluconeogenesis (the formation of new sugar) in the liver and the body is unable to counter-regulate. Alcohol also interferes with the perception of hypoglycemia and the corresponding cognitive functions. To avoid hypoglycaemia, the amount of carbohydrates in alcoholic beverages should not be taken into account in the insulin dosage. In non-diabetics may in chronic malnutrition z. B. in the context of a continued alcohol abuse to a lack of glucose in the liver and thus to hypoglycaemia.

When hypoglycaemia begins, the brain causes an increased output of adrenaline , since the release of adrenaline leads to an increase in the blood sugar level ( sympathetic activity ). At the same time, the liver is stimulated to release more glucose from glycogen (the storage form of glucose) and the pancreas stops producing insulin; in turn, the release of glucagon is increased. As a rule, the body's own regulatory measures are sufficient to prevent hypoglycaemia.

Because the brain is insufficiently supplied with glucose, neurological deficits are the first signs of acute hypoglycaemia. This can be accompanied by changes in personality, including aggressiveness. In the stage of deep hypoglycemia, unconsciousness occurs with the corresponding dangers.

The sympatho-adrenergic activation during hypoglycemia is primarily responsible for abnormal cardiac repolarization. When the adrenaline level is high due to acute hypoglycaemia, there are intense effects on the cardiovascular system. The result is an increased heart rate, increased systolic and decreased diastolic blood pressure. This can make an existing heart failure worse. The risk of cardiac ischemia due to hypoglycaemia is statistically significantly increased.

The hypoglycaemia factitia is a disease in which it is targeted by self-administration of hypoglycemic agents to an intentional lowering of blood sugar. It is an important differential diagnosis for all hypoglycaemia that occurs in diabetics and non-diabetics.

Hypoglycemia in the newborn

Newborns from poorly controlled diabetic mothers tend to have hypoglycaemia after birth. The cause is the high level of glucose in the mother's blood. The glucose reaches the fetus via the placenta . In response to the oversupply, the pancreas of the fetus produces excessive amounts of insulin. After the delivery, the mother's glucose disappears, but the cells of the child's pancreas have not yet changed and continue to produce more insulin than necessary. This means that the glucose in the blood is used up more quickly, and the newborn baby becomes hypoglycaemic.

Clinical manifestations

Reduced blood sugar levels do not have to lead to symptoms per se, even below 50 mg / dl. In diabetics, on the other hand, they can occur even at higher values.

Typical symptoms are cravings , nausea , vomiting and weakness or asthenia ( parasympathetic reactions), nervousness and restlessness, sweating , tachycardia , tremors , mydriasis and high blood pressure ( sympathetic reactions) as well as symptoms that are attributed to an influence on the central nervous system by the hypoglycaemia, such as headache , moodiness , personality changes, "irritability", poor concentration, slowing down, confusion, fear , (muscular) coordination disorders, primitive automatisms (e.g. grimacing, grasping and smacking) as well as focal signs (e.g. double vision and other visual disturbances, seizures , paralysis on one side , speech disorders and drowsiness ). The symptoms of hypoglycemia reach their maximum extent in hypoglycemic shock , which is associated with central respiratory and circulatory disorders ranging from unconsciousness to death. In emergency medicine , hypoglycaemia should be excluded if neurological or psychiatric abnormalities are unclear .

Hypoglycaemia under therapy is a major factor in the quality of life and life expectancy of diabetic patients. At 88%, severe hypoglycaemia is the most common emergency among acute diabetic complications.

Repeated severe hypoglycaemia has shown in a retrospective observational study in type 2 diabetics an increased risk of later development of dementia . In the case of severe hypoglycemia, the dementia rate increased by 26 percent in the observed patients according to the analysis of the medical records, in two episodes by 80 percent and in three hypoglycemia the dementia rate almost doubled. If the illness lasts for a long time, especially in type 2 diabetes with the frequent accompanying illnesses such as hypertension and coronary heart disease , hypoglycaemia increases the risk of life-threatening complications.

The hypoglycemia perception of type 2 diabetics is usually a misperception in the early phase of the disease. Since the body is used to increased blood sugar values ​​at the beginning of diabetes mellitus or when the metabolism is inadequate, even highly normal values ​​of 90 or 120 mg / dl are felt as hypoglycaemia. In the further phase of the disease, hypoglycaemia rarely occurs due to the counterregulation received and in particular due to the insulin resistance. Only in the late phase of type 2 diabetes can symptoms such as those found in type 1 diabetics occur if the self-production of insulin and the general increase in concomitant diseases fail.

  • Asymptomatic hypoglycaemia can also be more confirmed in type 2 diabetics at higher threshold values ​​(e.g. from 30.7% at threshold <3.1 mmol / l to 61.7% at threshold <3.9 mmol / l ( 70 mg / dl)). A loss of the warning signs of hypoglycaemia in the presence of autonomic neuropathy must be taken into account .
  • Counter-regulatory hormones are released by type 2 diabetics even at higher glucose levels than by comparable type 1 diabetics (e.g. ACTH at 3.7 mmol / l = 67 mg / dl) without the symptoms being aggravated.
  • The release of counter-regulatory hormones in response to hypoglycemia occurs in well-adjusted type 2 diabetics with normal glucose levels (e.g. epinephrine at 68 mg / dl = 3.8 mmol / l).
  • Type 2 diabetics are subject to counter-regulation before symptoms set in.

Acute symptoms of neonatal hypoglycaemia are tremor , irritability , lethargy , respiratory failure , poor drinking, muscular hypotension , hypothermia , high-pitched screaming and cerebral seizures.

Investigation methods

Different blood glucose meters suitable for rapid tests

The blood sugar is usually measured using capillary or venous blood. The device indicates the level of the blood sugar level in the units mg / dl (milligrams per deciliter) or in mmol / l ( millimoles per liter), where 1,000 mg / dl corresponds to approximately 0.05549 mmol / l.

In addition to an exact laboratory quantitative analysis (for example using the Hagedorn-Jensen method) as a rule, the most precise possible measurements of the magnitude of a hypoglycemia are important , especially in emergency situations , but also for self-control (semiquantitative analysis). Rapid tests are suitable for this, in which the blood is applied to a test strip and causes discoloration there. This discoloration is then read out optically using a blood glucose meter . There are also test strips that allow a meaningful assessment without tools, i.e. with the naked eye. In the blood, red blood cells typically use glucose. As a result, readings obtained from samples that have been stored improperly for a long time can have falsely low values.

If hypoglycemia is found in non-diabetics, this requires further clarification.


Acute hypoglycaemia can be ended briefly by adding carbohydrates (especially grape sugar). This can be done in a conscious patient with mild hypoglycaemia by giving 10 to 20 grams of glucose, sugary drinks (1 glass of apple or orange juice or cola), followed by slowly absorbable carbohydrates (about 1 to 2 KU bread) or appropriate food happen.

However, if unconsciousness has already occurred, no fluids or food may be administered orally, since the unconscious patient is at risk of aspiration due to intermittent swallowing reflexes . In the case of severe hypoglycemia, a doctor or rescue service employee therefore injects glucose directly intravenously , initially around 20 to 40 ml of 40% glucose; in unconscious patients, glucagon (0.5 to 1 mg) can also be used intravenously, subcutaneously or intramuscularly.

A trained helper can also give an intramuscular dose of glucagon to unconscious patients. Glucagon increases blood sugar by releasing glucose from the body's glycogen stores. However, glucagon does not work after the glycogen stores are exhausted, for example after consuming alcohol. After awakening, glucose is given orally (see above), at least 15 g of glucose are required.

In any case, in such a situation it is absolutely necessary to make an emergency call or to inform a doctor or rescue service.

  • The awake patient should eat 2 to 4 tablets (corresponds to 1 to 2 BE) glucose or the corresponding amount of a commercially available preparation or give 200 to 400 ml of fruit juice or other drinks containing carbohydrates to drink
  • If the person is unconscious, do not put glucose in the mouth (risk of aspiration)
  • Doctor or emergency services to communicate
  • Glucose intravenous (iv) (by healthcare professionals only)
  • Inject glucagon into the subcutaneous fat tissue or intramuscularly (in known diabetics, from interned persons)

Until the doctor arrives:

In the case of newborns, feeding is usually sufficient (application to the breast, feeding expressed breast milk, hydrolyzed formula or maltodextrin solution, possibly also via a gastric tube).

Prediction and Prevention

The continuous glucose measurement (rtCGM) made it possible to provide the user with additional information regarding the development of hypoglycemia by displaying the glucose trend (time gradient). Systems or algorithms based on CGM can be subdivided into those that interrupt the insulin supply and those that generate an alarm, which may prompt the user to eat more effective carbohydrates and thus carry out prevention. A distinction must again be made between: simple exceeding of limit values ​​and prediction . The former notifies the user when a critically low glucose concentration threshold is exceeded (e.g. 90 mg / dl), while the latter predicts a hypo-risk so that the user can, if necessary, consume fast-acting carbohydrates in advance in order to achieve the Avoid hypoglycemia. These systems require i. d. R a model of the patient to carry out such predictions digitally.

While the prediction horizon (forecast period) can be small during the day (usually 30 minutes), longer forecast periods are required at night (several hours), since it makes sense to take an action before going to sleep. It has been shown that false alarms that wake up the user reduce his willingness to wear such a device. Fortunately, less influencing factors such as physical activity and meals with insulin administration are common during the night, which makes predictions easier. Basically, as everywhere, the following applies: longer prediction horizon means worse forecast.


Studies can be used to determine hit rates (correctly identified hypoglycaemia) and false positives (false positives).

Switching off the continuous insulin supply by means of a pump requires longer forecast periods with uncertain prediction, since the cessation of the action of insulin is more delayed than the consumption of fast-acting carbohydrates. According to a meta-analysis , this method reduced nocturnal hypoglycaemia by an average of 8.8%.

By creating an individual patient model from historical CGM data, 85% (true positives) of the impending hypoglycaemia can be predicted in a prediction period of 40 minutes, while at the same time rates of false positives (false alarms) remain below 0.4%. However, the detection rates do not yet mean a clinically proven reduction in hypoglycaemia.

In the case of nocturnal hypoglycaemia, hypoglycaemia during the night (on average after 3.5 hours) could be predicted before going to sleep at a rate of 75%.

In type 2 diabetes, it was possible to show that discontinuous self-control measurements with the help of machine learning resulted in hypoglycaemia over a forecast period of 24 hours with a hit rate of 92% (correct positive, sensitivity) and a rate of false positives (1-specificity) of less than 30% can be predicted.

Literature and Sources

  • SA Amiel, T. Dixon, R. Mannt, K. Jameson: Hypoglycaemia in Type 2 diabetes. In: Diabetic Medicine. 25, 2008, ISSN  0742-3071 , pp. 245-254.
  • Richard Daikeler, Götz Use, Sylke Waibel: Diabetes. Evidence-based diagnosis and therapy. 10th edition. Kitteltaschenbuch, Sinsheim 2015, ISBN 978-3-00-050903-2 , p. 108.
  • Mehnert, Standl, Usadel, Häring (eds.): Diabetology in clinic and practice. 5th edition. Thieme, Stuttgart 2003, ISBN 3-13-512805-9 .
  • Silbernagl, Lang: Pocket Atlas of Pathophysiology. Thieme, Stuttgart 1998, ISBN 3-13-102191-8 .
  • Lothar Thomas: Laboratory and Diagnosis. Indication and evaluation of laboratory results for medical diagnostics. 7th edition. TH-Books Verlags-Gesellschaft, Frankfurt am Main 2008, ISBN 978-3-9805215-6-7 .
  • RA Whitmer et al .: Hypoglycemic episodes and risk of dementia in older patients with type 2 diabetes mellitus. In: JAMA. 301 (2009), pp. 1565-1572.

Web links

Individual evidence

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