DIABETES CASE PRESENTATIONS

1. DIABETES CASE PRESENTATIONS 2nd – Acute complications

2. 1. HYPOGLYCEMIA • Factors that precipitate or predispose to hypoglycemia: • Excessive insulin levels • Excessive dosage (error or deliberate overdose) • Increased insulin bioavailability • Accelerated absorption (exercise, injection into muscle) • Renal failure • “Honeymoon period” • Enhanced insulin effect • Increased insulin sensitivity • Counter-regulatory hormone deficiencies (Addison’s disease) • Weight loss • Physical training • Postpartum • Inadequate carbohydrate intake • Other factors • Exercise • Alcohol • Drugs

3. Consequences of decrease in blood glucose level

4. Signs and symptoms of hypoglycemia

5. Clinical classification of hypoglycemia • Mild – patients treat themselves • Moderate – patients need assistance from entourage for treatment • Severe – patients need medical assistance for treatment (unconscious)

6. Treatment of hypoglycemia • Preventive (avoidance of hypoglycemia): • Training in insulin-dose adjustment according to frequent blood glucose monitoring • “Blood glucose awareness training” • Curative: • Conscious patient: • Mild hypoglycemia: simple carbohydrates  complex carbohydrates • Moderate hypoglycemia: simple carbohydrates  glucagon  complex carbohydrates • Unconscious patient: • IV glucose (33%, 20%) • Glucagon 1 mg SC or IM All unconscious patients with insulin treatment should be treated as for severe hypoglycemia until proved otherwise

7. Hyperglycemia: - Diabetes mellitus - Hyperosmolar non-ketotic hyperglycemia - Stress hyperglycemia - IGT Metabolic acidosis: - Lactic acidosis - Uremic acidosis - Hiperchloric acidosis - Drog-induced acidosis DKA Ketosis: - Alcohol ketosis - Hunger ketosis 2. DIABETIC KETOACIDOSIS • DEFINITION: hyperglycemia + hyperketonaemia + metabolic acidosis

8. Pathophysiology of DKA Relative or total insulin deficiency Lipolisis Protein breakdown Hyperketonemia  Glicogenolisis and neoglucogenesis  alanine and other aminoacids Hyperglycemia and glycosuria Metabolic acidosis  urea Hyperosmolarity Osmotic polyuria Loss of water, K+, PO4-, HCO3- Dehidration Thirst Arrhythmia Colaps Polidipsia COMA

9. Precipitating factors for DKA • Total insulin deficiency: • errors and omissions in administrating insulin • new cases of diabetes • Relative insulin deficiency: • acute illnesses: • infections • macrovascular disease (myocardial infarction, stroke) • surgical or traumatic stress • endocrine diseases (tireotoxicosis, Cushing’s syndrome) • drugs (steroids) • pregnancy • stress

10. Signs and symptoms of DKA • Signs of dehydration: • dry skin and mucosa • hypothermia • tachicardia • arterial hypotension – 10% of cases! • polyuria → oligoanuria • Respiratory signs: Küssmaul respiration, odour of acetone on pacient’s breath • Digestive signs: nausea and vomiting, abdominal pain • Neuro-muscular signs: muscular weakness, ↓ / absent reflexes • Consciousness: confusion and drowsiness (coma in 10% of cases)

11. hyperglycemia hyperketonemia HCO3- ↓, pH ↓ hydro-electrolytic unbalance anionic gap: (Na+ + K+) – (Cl- + HCO3- + 16) ↑ urea hemoconcentration, ↑ WBC glucosuria hyperketonuria ECG  cardiac enzymes chest X-ray abdominal ultrasonography blood, urine and sputum for culture Average hydro-electrolytic losses: fluid: 5 – 10 L (up to 10% of weight) HCO3- : 800 – 1000 mEq K+: 300 – 600 mEq (K+ intracelular → extracelular!) Na+ : 400 – 600 mEq Mg++: 50 – 75 mEq Ca++: 1000 – 1500 mEq P: 75 – 150 mEq Laboratory investigations

12. Stages of DKA

13. Treatment of ketosis • no digestive symptoms • hyperglycemia > 250 – 300 mg/dl (for > 12 hours) → determine ketonuria, monitor blood glucose levels frequently • if T2DM with diet and oral drugs→ temporary insulin treatment • if T2DM with insulin treatment + moderate ketonuria (+ - ++) → increase doses and /or frequency of insulin injections • if T2DM with insulin treatment + marked ketonuria (+++ - ++++) → → rapid-acting insulin SC every 2 hours until blood glucose level back to normal • oral rehydration (salty liquids, electrolytes intake)

14. Treatment of DKA (1) 1. Fluids and electrolytes: • Saline: • 0 – 1 h = 1000 – 1500 ml • 1 – 4 h = 500 – 1000 ml/h • Glucose: • 5%, 10% when blood glucose level < 250 – 300 mg/dl + rapid acting insulin (1 U/2g glucose or 1 U/3g of glucose) • KCl: • K > 5 mmol/L : do not add K → monitor! • K = 3,5 – 5 mmol/L : 20 mmol/h • K < 3,5 mmol/L : 40 mmol/h

15. Treatment of DKA (2) 2. Insulin: • rapid-acting insulin – IV 0,1 u/kg/h (or continuous intravenous infusion) • a decrease of 75 – 100 mg/dl in blood glucose level/hour is sufficient • insufficient decrease  increase the dose of insulin 3. Sodium bicarbonate • pH < 7,1 • give with extreme care • pH < 6,9 : max. 600 ml Na HCO3- 1,4% or 100 ml Na HCO3- 8,4% • pH = 6,9 – 7 : 300 ml Na HCO3- 1,4 % or 50 ml Na HCO3- 8,4 % • pH > 7,1: STOP • risc of cerebral oedema!

16. Treatment of DKA (3) 4. Treatment of hypotention • if BP < 100 mmHg after 2 h of treatment • HHC 100 – 200 mg • macromolecular solutions • plasma 5. Treatment of infections • antibiotics 6. Other measurements • oxygen • urinary catheter if conscious level impaired or no urine passed after 4 h of treatment • nasogastric tube if risc of aspiration • heparine 5000u/8h 7. Treatment of precipitating cause

17. 3. HYPEROSMOLAR NON-KETOTIC HYPERGLYCEMIA • Diagnosis criteria: • osmolarity > 350 mOsm/l • blood glucose level > 630 mg/dl • pH > 7,25 • HCO3- > 15 mEq/l • extreme dehydration • Calculating osmolarity: • 2[Na+(mmol/L) + K+(mmol/L)] + glycemia (mmol/L) + urea (mmol/L) • 2[Na+(mmol/L) + K+(mmol/L)] + glycemia (mg/dl)/18 + urea (mg/dl)/6