Pathogenesis (disease development) of ketoacidotic coma
In ketoacidotic coma, absolute insulin deficiency causes simultaneous hyperglycemia (hyperglycemia; glucose: > 250 and < 600 mg/dl) and lipolysis (mobilization of fat reserves), which in turn leads to hypovolemia (amount of blood in the body ↓) and metabolic acidosis (metabolic acidosis of the blood) via hyperosmolarity and ketosis.
Etiology (causes) of ketoacidotic coma
Behavioral causes
- Dietary errors
Disease-related causes
Endocrine, nutritional and metabolic diseases (E00-E90).
- Initial manifestation of type 1 diabetes – in circa 25% of cases, ketoacidotic coma is the first sign of type 1 diabetes mellitus (manifestation coma)
- Hyperthyroidism (hyperthyroidism) – leads to increased insulin requirements.
Cardiovascular system (I00-I99)
Infectious and parasitic diseases (A00-B99).
- Infections lead to increased insulin requirements; they are the most common trigger, accounting for circa 40%.
Mouth, esophagus (esophagus), stomach, and intestines (K00-K67; K90-K93).
- Diseases of the gastrointestinal tract – lead to increased insulin requirements.
Pregnancy, childbirth and puerperium (O00-O99).
- Pregnancy – leads to increased insulin requirements.
Injuries, poisoning, and other consequences of external causes (S00-T98).
- Injuries, accidents – lead to increased insulin requirementsEMA warns of possible toe amputations after taking the SGLT2 inhibitor canangliflozin.
Medication
- Insufficient insulin therapy
- Medication error
- Therapy with:
- Glucocorticoids
- Diuretics (diuretic medications).
- SGLT2 inhibitors such as canagliflozin, dapagliflozin, and empagliflozinEMA warns of possible toe amputations after taking the SGLT2 inhibitor canangliflozinFDA warns of Fournier’s gangrene caused by SGLT2 inhibitors
Pathogenesis (disease development) of hyperosmolar coma
In hyperosmolar coma, decreased peripheral glucose utilization occurs due to relative insulin deficiency. At the same time, however, there is also increased glucose release from the liver. Hyperglycemia (hyperglycemia; glucose: > 600 to well over 1,000 mg/dl) leads to osmotic polyuria (caused by blood glucose concentrations above 180 mg/dl (renal threshold), which causes the reabsorption capacity of the tubular system to be exceeded, resulting in glucosuria (increased excretion of glucose in the urine) and thus increased water excretion (polyuria)). This in turn leads to hypovolemia (amount of blood in the body ↓) or severe desiccosis (dehydration). However, since small amounts of insulin are still released, ketosis does not occur.
Etiology (causes) of hyperosmolar coma
Behavioral causes
- Nutrition:
- Intake of excessive amounts of glucose-containing beverages (fruit juices, cola, etc.).
Infectious and parasitic diseases (A00-B99).
- Gastroenteritis (gastrointestinal flu) – leads to large fluid losses.
- Infections – lead to increased insulin requirements; they represent the most common trigger with circa 40%.
Cardiovascular system (I00-I99)
- Cardiovascular complications, unspecified.
Mouth, esophagus (food pipe), stomach, and intestines (K00-K67; K90-K93).
- Gastrointestinal diseases (with vomiting, severe diarrhea/diarrhea) – lead to increased insulin requirements.
Symptoms and abnormal clinical and laboratory findings not elsewhere classified (R00-R99).
- Impaired thirst sensation
- Large fluid losses during heavy sweating or fever
Genitourinary tract (kidneys, urinary tract – sex organs) (N00-N99)
Medications
- Inadequate uncontrolled intravenous administration of isotonic or hypertonic solutions (e.g., hyperalimentation)
- Therapy with diuretics* , certain psychotropic drugs* , glucocorticoids, protease inhibitors.
* See Drug side effects/Diabetogenic effect due to drugs.
