Premise
The complications of diabetes (or diabetes mellitus ) are the unpleasant consequences that can arise from this serious metabolic disease.
Diabetes is caused by a deficiency of insulin - a key hormone for maintaining normal blood glucose levels - and its characteristic clinical sign is the high concentration of glucose in the blood ( hyperglycemia ).
Reminding readers that the most known and widespread types of diabetes are type 1 diabetes and type 2 diabetes; this article aims to treat the possible acute complications of the two aforementioned types of diabetes.
Acute complications
The acute complications of type 1 and type 2 diabetes are diabetic ketoacidosis and non-ketotic hyperosmolar coma (or simply hyperosmolar coma ).
To be more precise, diabetic ketoacidosis most often characterizes type 1 diabetes, while hyperosmolar coma most frequently distinguishes type 2 diabetes.
The term "acute", referring to these complications, refers to their sudden and sudden onset, following their specific triggering event (which will be discussed in the next chapters of the article).
Brief review of the causes of type 1 diabetes and type 2 diabetes
- The cause of type 1 diabetes is a reduced availability of insulin, due to the loss, due to autoimmune destruction, of the pancreatic cells responsible for the production of this hormone.
- The possible causes of type 2 diabetes are the insensitivity of the tissues to the action of insulin and the progressive decline, up to the complete loss, of the own capacity of some cells of the pancreas (to be precise, the beta cells of the Langerhans islands) to produce insulin.
Diabetic ketoacidosis
Diabetic ketoacidosis is a potentially lethal complication of diabetes, which arises from insulin deficiency (or reduced availability of insulin ) and from excess glucagon, two typical circumstances of type 1 diabetes (and this explains why diabetic ketoacidosis is more frequent in this type of diabetes).
How is diabetic ketoacidosis established?
Insulin is the hormone that promotes the entry of glucose into the tissues of the human body; for body cells, glucose is the main source of energy .
When there is a lack of insulin, as in type 1 diabetes, glucose can no longer enter cells, which, consequently, lack their preferred energy resource.
To cope with this situation, therefore, the organism is forced to lean on an alternative energy source, otherwise it would die. Here then is that he uses lipids .
In order to obtain energy from lipids, the body must transfer the latter to a site equipped for the aforementioned purpose: the liver with its hepatocytes .
In the liver, the process that involves the generation of energy from lipids is the so-called oxidation of fatty acids .
Oxidation of fatty acids is a complex biological phenomenon, which produces energy and in parallel a molecule called acetyl-coenzyme A. Acetyl coenzyme A is the starting molecule for the formation of the so-called ketone bodies (acetone, beta-hydroxybutyric acid and acetoacetic acid).
While in the healthy person the ketone bodies are quantitatively modest and maintained under control through the elimination of urine (in which they are removed), in the type 1 diabetic - where the oxidation of fatty acids is the only energy source - the ketone bodies represent such a massive presence, that its complete and correct elimination through the urine is impossible.
The permanence, due to lack of excretion through the urine, of the ketone bodies in the body causes these dangerous molecules to accumulate in the blood.
The accumulation in the blood of the diabetic of ketone bodies is the pathological phenomenon that, in the medical field, establishes the beginning and the establishment of the condition of diabetic ketoacidosis.
The key points of why and how ketoacidosis is established in type 1 diabetic
- In type 1 diabetics, ketoacidosis depends on insulin deficiency;
- Without insulin, the body's cells lack their main source of energy: glucose;
- To compensate for the lack of glucose and its energy, the body is forced to exploit the energetic content of lipids;
- To obtain energy from lipids, the organism transfers the latter into the liver and subjects them to the so-called oxidation of fatty acids;
- In generating energy, the oxidation of fatty acids also produces large amounts of acetyl-coenzyme A, the molecule from which the ketone bodies are derived (acetone, beta-hydroxybutyric acid and acetoacetic acid);
- If the ketone bodies are a massive presence, as in the case of the type 1 diabetic, their complete elimination with urine is impossible;
- The failure to eliminate the ketone bodies with urine, due to their high concentration, leads to their accumulation in the blood;
- The accumulation in the blood of ketone bodies marks the beginning of the condition of diabetic ketoacidosis.
What are the symptoms of diabetic ketoacidosis?
The first symptoms of diabetic ketoacidosis are gastrointestinal disorders, such as anorexia (lack of appetite), nausea, vomiting and abdominal pain. Therefore, to these gastrointestinal disorders, at a later stage, other manifestations are added, including: confusion, weakness, severe increase in urination, deep breathing, sense of fainting and fainting.
Important: what NOT to do when the first symptoms of diabetic ketoacidosis appear?
The most common mistake that diabetics make at the onset of diabetic ketoacidosis is to suspend the administration of insulin, as a result of the fact that gastrointestinal disorders, of which the patients are victims, prevent them from taking regular meals.
This is an absolutely wrong choice, because taking insulin is the only real solution to the problem that is about to emerge; indeed, just to understand the importance of insulin, the intake of the insulin should undergo an increase compared to those that are the usual doses, if you want to avoid the worst.
Therefore, in conclusion, it is the failure to administer insulin, just when it would be essential to increase its dose, the main event on which the further evolution of ketoacidosis depends.
Complications of diabetic ketoacidosis
If not adequately treated, diabetic ketoacidosis degenerates and progresses to the so-called ketoacidosic coma, in which the patient has a deep and rapid breath (the so-called Kussmaul breath ), a breath that intensely smells of rotten fruit (the so-called acetonic breath ), a profoundly dehydrated appearance, sunken eyeballs, dry and chapped lips, intense glycosuria, large quantities of ketone bodies in urine and blood, and high hyperglycemia (between 500 and 700 mg / ml).
Ketoacidosic coma is a serious medical condition, which can lead to the death of the person concerned.
Hyperosmolar coma
Potentially lethal like diabetic ketoacidosis, hyperosmolar coma is the serious medical condition in which the cases of type 2 diabetes generally characterized by a prolonged and severe hyperglycaemia generally result.
The severe hyperglycemia that characterizes hyperosmolar coma has two important consequences:
- the large increase in plasma osmolarity, due to the high concentration of glucose in the blood,
- cellular dehydration, due to a significant worsening of polyuria (one of the typical symptoms of diabetes mellitus).
Hyperosmolar coma is characteristic of elderly diabetic patients. Sensing the sense of thirst less efficiently due to age, in fact, elderly patients with type 2 diabetes tend to take less water than what the state of polyuria deserves, and to develop, precisely because of the reduced fluid intake, severe hyperglycemia.
From the hyperosmolar coma - in particular, from the deriving state of cellular dehydration - a serious neurological symptomatology follows, which includes:
- Convulsions;
- Engine deficits;
- Focal epilepsy crisis;
- Muscle tremors and / or fasciculations;
- Muscular flaccidity;
- Alteration of reflexes;
- Alteration of the state of consciousness;
- Hallucinations.
Furthermore, these neurological symptoms may be accompanied by other disorders, such as: dry mouth, intense thirst, hot skin without sweat, fever, vision problems, nausea, drowsiness, respiratory infections, thrombosis and pancreatitis.
As can be guessed from the term "non-ketose", the non-ketose hyperosmolar coma differs from diabetic ketoacidosis due to the absence of ketone bodies ; after all the latter depend on the absolute deficiency of insulin, which is not a prerogative of type 2 diabetes.
Curiosity: all the names of the non-ketosic hyperosmolar coma
Non-ketosic hyperosmolar coma is also known by other names. In addition to hyperosmolar coma, it is also said: hyperglycemic-hyperosmolar state, non-ketosic hyperglycemic-hyperosmolar coma, non-ketosic hyperosmolar syndrome and hyperosmolar diabetic syndrome.
Which values does hyperglycemia reach in hyperosmolar coma?
In hyperosmolar coma, the values of hyperglycemia are at least higher than 600 mg / ml and, in most cases, even exceed 1, 000 mg / ml (therefore almost double what can be observed in diabetic ketoacidosis).
What clinical signs characterize hyperosmolar coma?
In addition to high hyperglycemia, laboratory tests on a hyperosmolar coma patient show:
- Marked glycosuria, in the absence of ketone bodies;
- Increased viscosity of the blood (on which the thrombosis phenomena depend);
- Serum pH levels above 7.30;
- Plasma osmolarity above 320 mOsm / kg.
What are the consequences of non-ketose hyperosmolar coma?
If not treated promptly and appropriately, hyperosmolar non ketosic syndrome degenerates until the patient enters a state of coma (NB: in this case, a coma means a state of unconsciousness).
The coma resulting from the non-ketosic hyperosmolar syndrome represents a very serious medical circumstance, from which, with high probabilities, the death of the patient can arise.
