Final acute complications of diabetes mellitus
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This document discusses the acute complications of diabetes mellitus, including diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar coma (HNC), lactic acidosis (LA), and hypoglycemia. It provides information on the precipitating factors, signs and symptoms, laboratory findings, and treatment for each complication. The treatment sections emphasize rehydration, reducing hyperglycemia and correcting electrolyte and acid-base imbalances. Insulin therapy is also discussed for DKA and LA.
Final acute complications of diabetes mellitus
- 1. ACUTE COMPLICATIONS OF DIABETES MELLITUS Dr.Sandeep yadav
- 2. ACUTE COMPLICATIONS OF DIABETES MELLITUS
- 3. 1)Diabetic ketoacidisis • Precipitating factors • Signs, symptoms, physical examination, laboratory findings • Treatment 2)Non ketotic hyperglycemic hyper osmolar coma • Precipitating factors • Signs, symptoms, physical examination, laboratory findings • Treatment 3)Lactoacidosis • Precipitating factors • Signs, symptoms, physical examination, laboratory findings • Treatment 4)Hypoglycemic AND Hypoglycaemic coma • Precipitating factors • Signs, symptoms, physical examination, laboratory findings • Treatment
- 4. Hyperglycemia Ketosis Acidosis * Adapted from Kitabchi AE, Fisher JN. Diabetes Mellitus. In: Glew RA, Peters SP, ed. Clinical Studies in Medical Biochemistry. New York, NY: Oxford University Press; 1987:105. Definition of Diabetic Ketoacidosis* 4
- 5. Precipitating factors of DKA
- 6. • Newly Diagnosed Diabetes (Presenting Manifestation • Inadequate Administration Of Exogenous Insulin; ABSOLUTE INSULIN DEFICIENCY • Inadequate Administration Of Exogenous Insulin • An Intercurrent Infection (Pneumonia, Cholecyctitis); • A Vascular Disorder (Myocardial Infarction, Stroke); • An Endocrine Disorder(hyperthyroidism, Pheochromocytoma); • Trauma; • Pregnancy; • Surgery RELATIVE INSULIN DEFICIENCY
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- 8. Electrolyte LossesRenal Failure Shock CV Collapse Insulin Deficiency 8 Hyperglycemia Hyper- osmolality Δ MS Glycosuria Dehydration
- 10. Electrolyte LossesRenal Failure Shock CV Collapse Insulin Deficiency 10 Hyperglycemia Hyper- osmolality Δ MS Lipolysis FFAs Acidosis Ketones CV Collapse Glycosuria Dehydration
- 11. Diabetic Ketoacidosis: Pathophysiology Unchecked gluconeogenesis Hyperglycemia Osmotic diuresis Dehydration Unchecked ketogenesis Ketosis Dissociation of ketone bodies into hydrogen ion and anions Anion-gap metabolic acidosis 11 • Often a precipitating event is identified (infection, lack of insulin administration)
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- 13. Clinical Presentation of Diabetic Ketoacidosis History Physical Exam • Thirst • Polyuria • Abdominal pain • Nausea and/or vomiting • Profound weakness • Kussmaul respirations • Fruity breath • Relative hypothermia • Tachycardia • Supine hypotension, orthostatic drop of blood pressure • Dry mucous membranes • Poor skin turgor 13
- 14. Initial Laboratory Evaluation of DKA • Comprehensive metabolic profile • Serum osmolality • Serum and urine ketones • Arterial blood gases • CBC • Urinalysis • ECG 14
- 15. Treatment REFERENCES: 1) American Diabetic Association 2) British Medical Journal 3) E-medscape 4) Harisson Principle Of Internal Medicine 18th Edition 5) British Society Of Paediatric Endocrinology
- 16. The goals of therapy include: 1.Rehydration 1.Reduction of hyperglycemia 2.Correction of electrolyte imbalance 3. Correction of acid-base imbalance 4.Investigation of precipitating factors, treatment of complications.
- 17. FLUIDS FLUID RESUSCITATION IS A CRITICAL PART OF TREATING PATIENTS WITH DKA. Intravenous solutions replace extravascular and intravascular fluids and electrolyte losses. They also dilute both the glucose level and the levels of circulating counterregulatory hormones. Fluid it self leads to correction of acidosis to some extent Insulin is needed to help switch from a catabolic state to an anabolic state, with uptake of glucose in tissues and the reduction of gluconeogenesis as well as free fatty acid and ketone production
- 18. 0.9 % NaCl(15-20 ml/kg/hr) Administer 1-3 L during the first hour. Administer 1 L during the second hour Administer 1 L during the following 2 hours Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings
- 19. In general, 0.45% NaCl infused at 4–14 ml · kg−1 · h−1 is appropriate if the corrected serum sodium is normal or elevated
- 21. In adult patients, (IfK+ <3.3 mEq/l) , an IV bolus of regular insulin at 0.15 u/kg body wt continuous infusion of regular insulin at a dose of 0.1 unit · kg−1 · h−1 (5–7 units/h in adults), should be administered If plasma glucose does not fall by 50 mg/dl from the initial value in the 1st hour, check hydration status; if acceptable, the insulin infusion may be doubled every hour until a steady glucose decline between 50 and 75 mg/h is achieved. When the plasma glucose reaches 250 mg/dl in DKA or 300 mg/dl in HHS, it may be possible to decrease the insulin infusion rate to 0.05–0.1 unit · kg−1 · h−1 (3–6 units/h), and dextrose (5– 10%) may be added to the intravenous fluids. Initiate subcutaneous insulin at least 2 h before interruption of insulin infusion
- 22. Potassium Repletion in DKA • K+ >5.2 mEq/L ▫ Do not give K+ initially, but check serum K+ with basic metabolic profile every 2 h ▫ Establish urine output ~50 mL/hr • K+ <3.3 mEq/L ▫ Hold insulin and give K+ 20-30 mEq/hr until K+ >3.3 mEq/L • K+ = 3.3-5.2 mEq/L ▫ Give 20-30 mEq K+ in each L of IV fluid to maintain serum K+ 4-5 mEq/L 22
- 23. Phosphorus Repletion in DKA • A sharp drop of serum phosphorus can also occur during insulin treatment • Treatment is usually not required ▫ Caregiver can give some K+ as K- phos 23
- 24. CORRECTION OF ACID BASE BALANCE Its role is controversial Sodium bicarbonate only is infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis It is recommended for patients in shock and/or if pH is <6.9
- 25. Treatment of Concurrent Infection • In the presence of infection, the administration of proper antibiotics is guided by the results of culture and sensitivity studies. Starting empirical antibiotics on suspicion of infection until culture results are available may be advisable.
- 27. Criteria for resolution of DKA glucose <200 mg/dl, serum bicarbonate ≥18 mEq/l, and venous pH of >7.3. Once DKA is resolved, if the patient is NPO, continue intravenous insulin and fluid replacement and supplement with subcutaneous regular insulin as needed every 4 h.
- 28. 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.
- 30. Physical examination 1. Severe dehydration is invariably present. 2. 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. 3. Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.
- 31. Laboratory findings 1. Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and over are common. 2. A markedly elevated serum osmolality is present, usually in excess of 350 mOsm/l. (Normal = 290 mOsm) 3. Serum ketones are usually not detectable, and patients are not acidic. 4. Serum sodium may be high (if severe degree of dehydration is present), normal, or high 5. Serum potassium levels may be high (secondary to the effects of hyperosmolality) Low or normal
- 32. DKA and HHS Are Life-Threatening EmergenciesDiabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Plasma glucose >250 mg/dL Plasma glucose >600 mg/dL Arterial pH <7.3 Arterial pH >7.3 Bicarbonate <15 mEq/L Bicarbonate >15 mEq/L Moderate ketonuria or ketonemia Minimal ketonuria and ketonemia Anion gap >12 mEq/L Serum osmolality >320 mosm/L 32
- 33. 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.
- 34. 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 1 mmol/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.
- 35. Predisposing factors 1. Heart and pulmonary failure (which leads to hypoxia) 2. Alcohol intoxication. 3. Ketoacidosis (it is important to have a very high index of suspection with respect to presence of LA).
- 36. Physical examination 1. Acrocyanosis is common. 2. Tachycardia frequently is present, blood pressure is decreased. 3. Poor skin tugor and dry skin may be prominent. 4. Hypothermia is common in LA. 5. Hyperpnea or Kussmaul respiration are present and related to degree of acidosis. 6. Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.
- 37. Laboratory findings 1. Blood glucose level is not high 2. Glucosurea is absent. 3. Blood lactic acid is high.
- 38. Treatment of LA LA is treated by correcting the underlying cause. 1. Oxygentherapy 2. Metyleneblue (50 – 100 ml of 1 % solution i/v droply) 3. In severe cases, bicarbonate therapy should be used (intravenously-infused 2,5 % sodium bicarbonates 1 to 2 l/day). 4. LA can be treated with low dose insulin regimens with 5 % glucose solution infusion. 5. 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)
- 39. Comparison of DCA, HNC and LA.
- 40. 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.
- 41. Precipitating factors • irregular ingestion of food; • extreme activity; • alcohol ingestion; • drug interaction; • liver or renal disease; • hypopituitarism and adrenal insufficiency.
- 43. Physical examination 1. The skin is cold, moist. 2. Hyperreflexia can be elicited. 3. Hypoglycemic coma is commonly associated with abnormally low body temperature 4. Patient may be unconsciousness.
- 44. Treatment • The most effective treatment of an insulin reaction is the immediate ingestion of a concentrated carbohydrate source, such as sugar, honey, candy, or orange juice. • Alternative methods for increasing blood glucose may be required when the person having the reaction is unconscious or unable to swallow: ▫ Glucagon may be given intramuscularly or subcutaneously. ▫ In situations of severe or life-threatening hypoglycemia, it may be necessary to administer glucose intravenously.
- 45. PREVENTION IS BEST CURE