1. ACUTE COMPLICATIONS OF DIABETES MELLITUS
Department of Internal Medicine №2
as.- prof. Martynyuk L.P.

2. Plan of lecture Diabetic ketoacidisis
Precipitating factors
Signs, symptoms, physical examination, laboratory findings
Treatment
Nonketonic hyperglycemic-hyperosmolar coma
Lactoacidosis
Hypoglycemic coma
Plan of lecture

3. Classification of acute complications of DM
1. Diabetic coma:
1) ketosis→diabetic ketoacidisis (DKA)
2) nonketonic hyperglycemic-hyperosmolar coma (NKHHC)
3) lactoacidosis (LA)
2. Hypoglycemic coma (HC)

4. Precipitating factors of DKA
1. newly diagnosed diabetes (presenting manifestation);
2. inadequate administration of exogenous insulin;
3. increased requirements for insulin caused by the presence of an underlying stressful condition:
an intercurrent infection (pneumonia, cholecyctitis);
a vascular disorder (myocardial infarction, stroke);
an endocrine disorder(hyperthyroidism, pheochromocytoma);
trauma;
pregnancy;
surgery

9. The goals of therapy include:
Treatment
The goals of therapy include:
Reduction of hyperglycemia
Rehydratation
Correction of electrolyte imbalance
Correction of acid-base imbalance
Investigation of precipitating factors, treatment of complications.

11. Nonketonic hyperglycemic-hyperosmolar coma (NKHHC or HNC).
HNC is a syndrome characterized by impaired consciousness, sometimes accompanied by seizures, extreme dehydration, , and extreme hyperglycemia that is not accompanied by ketoacidosis.

12. Predisposing factors
HNC seems to occur spontaneously in about 5 – 7 % of patients.
Infection (e.g., pneumonia, urinary tract infection, gram-negative sepsis) is underlying frequent precipitating cause.
Use of certain drugs has been associated with this condition:
steroids increase glucogenesis and antagonize the action of insulin;
potassium-wasting diuretics (hypokalemia decreases insulin secretion), e.g., thiazides, furosemide;
other drugs, e.g., propranolol, azathioprine, diazoxide.
Other medical conditions such as cerebrovascular accident, subdural hematoma, acute pancreatitis, and severe burns have been associated with HNC.
Use of concentrated glucose solutions, such as used in peripheral hyperalimentation or renal dialysis, has been associated with HNC.
HNC can be induced by peritoneal or hemodialysis, tube feeding.

13. Physical examination Severe dehydration is invariably present.
Various neurologic deficits (such as coma, transient hemiparesis, hyperreflexia, and generalized areflexia) are commonly present. Altered states of consciousness from lethargy to coma are observed.
Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.

14. Laboratory findings
Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and over are common.
A markedly elevated serum osmolality is present, usually in excess of 350 mOsm/l. (Normal = 290 mOsm/l).
The initial plasma bicarbonate averaged.
Serum ketones are usually not detectable, and patients are not acidic.
Serum sodium may be high (if severe degree of dehydration is present), normal, or high (when the marked shift of water from the intracellular to the extracellular space due to the marked hyperglycemia is present).
Serum potassium levels may be high (secondary to the effects of hyperosmolality as it draws potassium from the cells), normal, or low (from marked urinary losses from the osmotic diuresis). But potassium deficiency exists.

15. The goals of therapy include:
Treatment
This condition is a medical emergency and the patient should be placed in an intensive care unit.
Many of the management techniques recommended for a patient with DKA are applicable here as well.
The goals of therapy include:
rehydration;
reduction of hyperglycemia;
electrolytes replacement;
investigation of precipitating factors, treatment of complications.

16. Lactic acidosis (LA).
DM is one of the major causes of LA, a serious condition characterized by excessive accumulation of lactic acid and metabolic acidosis.
The hallmark of LA is the presence of tissue hypoxemia, which leads to enhanced anaerobic glycolysis and to increased lactic acid formation.
The normal blood lactic acid concentration is 1mmol/l, and the pyruvic to lactic ratio is 10:1. An increase in lactic acid without concomitant rise in pyruvate leads to LA of clinical importance.

17. Predisposing factors
Heart and pulmonary failure (which leads to hypoxia).
Usage of bigyanids.
Alcohol intoxication.
Ketoacidosis (it is important to have a very high index of suspection with respect to presence of LA).

18. Physical examination Acrocyanosis is common.
Tachycardia frequently is present, blood pressure is decreased.
Poor skin tugor and dry skin may be prominent.
Hypothermia is common in LA.
Hyperpnea or Kussmaul respiration are present and related to degree of acidosis.
Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.

19. Laboratory findings Blood glucose level is not high
Glucosurea is absent.
Blood lactic acid is high.

20. Treatment of LA LA is treated by correcting the underlying cause.
Oxygentherapy
Metylen blue (50 – 100 ml of 1 % solution i/v droply)
In severe cases, bicarbonate therapy should be used (intravenously-infused 2,5 % sodium bicarbonates 1 to 2 l/day).
LA can be treated with low dose insulin regimens with 5 % glucose solution infusion.
Symptomatic therapy:
Hydrocortisone (250 mg i/v)
Unitiol (5% solution 10 ml i/v (1- 2 ml/10 kg)
α-lipoid acid (berlition, espa-lipon)

21. Comparison of DCA, HNC and LA.

22. Hypoglycemia
It is a syndrome characterized by symptoms of sympathetic nervous system stimulation or central nervous system dysfunction that are provoked by an abnormally low plasma glucose level.
Hypoglycemia represents insulin excess and it can occur at any time.

23. Precipitating factors
irregular ingestion of food;
extreme activity;
alcohol ingestion;
drug interaction;
liver or renal disease;
hypopituitarism and adrenal insufficiency.

25. Physical examination The skin is cold, moist.
Hyperreflexia can be elicited.
Hypoglycemic coma is commonly associated with abnormally low body temperature
Patient may be unconsciousness.

26. Laboratory findings
Low level of blood glucose

27. Treatment

28. Treatment

29. References.
The Merck Manual of Diagnosis and Therapy (seventeenth Edition)/ Robert Berkow, Andrew J. Fletcher and others. – published by Merck Research Laboratories, – P
Manual of Endocrinology and Metabolism (Second Edition)/ Norman Lavin. – Little, Brown and Company.- Boston-New York-Toronto-London, P
Endocrinology (A Logical Approach for Clinicians (Second Edition)). William Jubiz.-New York: WC Graw-Hill Book, P. 241 – 253.