DIABETES CASE PRESENTATIONS 2nd – Acute complications

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

Consequences of decrease in blood glucose level ~ 85 mg/dl inhibition of insulin secretion ~60 – 70 mg/dl acute release of counter-regulatory hormones “alarm” symptoms ~50 – 60 mg/dl cognitive function deterioration (neuroglycopenia) ~20 mg/dl coma/seizure

Signs and symptoms of hypoglycemia Adrenergic (Autonomic) Neuroglycopenic tremor palpitations anxiety sweating hunger confusion drowsiness speech difficulty weakness incoordination headache visual disturbance behavior changes convulsions loss of consciousness

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

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

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

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 Colaps Arrhythmia Polidipsia COMA

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

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)

Laboratory investigations 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

Stages of DKA DKA HCO3- (mmol/L) pH Ketosis 21 - 24 normal Moderate DKA 16 - 20 7,31 – 7,35 Advanced DKA 11 - 15 7,30 – 7,21 Severe DKA ≤ 10 ≤7,20

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)

Treatment of DKA (1) 1. Fluids and electrolytes: Saline: Glucose: KCl: 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

Treatment of DKA (2) 2. Insulin: 3. Sodium bicarbonate 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!

Treatment of DKA (3) 5. Treatment of infections 6. Other measurements 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

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