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
~ 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

4. 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

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. 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

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
Colaps
Arrhythmia
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. Laboratory investigations
hyperglycemia
hyperketonemia
HCO3- ↓, pH ↓
hydro-electrolytic unbalance
anionic gap:
(Na+ + K+) – (Cl- + HCO )
↑ 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

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

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: 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

15. 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!

16. 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

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