Diabetic Emergencies

1. Diabetic Emergencies Emergency Block

2. DKADKA PATHOPHYSIOLOGY • Severe insulin deficiency • increased glucagon promotes lipolysis • Results in a massive increase in ketogenesis

3. KETONES ACETOACETATE ACETONE β HYDROXY BUTYRATE <1.5mmol/l More than 3mmol/l in blood DIABETIC EMERGENCIES

4. Pathophysiology

5. Who gets DKA? • Hallmark of type 1 diabetes • Previously undiagnosed DM (about 25 – 30%) • Interruption to normal insulin regime • Intercurrent illness - usually infection

6. Symptoms and signs • Nausea • Vomiting • Abdominal pain • Preceding polyuria, polydipsia, weight loss • Drowsiness/confusion/coma • Kussmaul respiration - hyperventilation • ‘Pear drops’ breath • Sign of infection or assoc disease _ (MI, pancreatitis)

7. How do I diagnose DKA? Diagnosis requires all 3 of the following: • Ketonaemia 3 mmol/L and over or significant ketonuria (more than 2+ on standard urine sticks) • Blood glucose over 11 mmol/L or known diabetes mellitus • Bicarbonate (HCO3- ) below 15 mmol/L and/or venous pH less than 7.3

8. Investigations • Bloods • FBC, UE, HCO3, LFT, CRP, Glu, cultures, amylase, cardiac enzymes, Blood ketones • Urine • Ketones, MSU • ABG • Initially only (lab HCO3 after) • CXR • ECG

9. Patient 1 pH 7.35 pCO2 3.2 pO2 16.0 HCO3 16.1 Patient 2 7.1 2.1 9.1 11.2 Example ABG

10. Treatment priorities • Replace fluids • Replace electrolytes • Replace insulin • Look for cause • Close monitoring

11. Initial management 1L 0.9% NaCl 30 mins 1hr 2hr 4 hr Then continue NaCl 0.9% as dictated by fluid status Later Slow NaCl and run 5% dextrose concurrently when gluc <15mmol If gluc normal but still ketones continue steady insulin with 5% or 10% dextrose (avoids recurrent DKA) Replacing fluids

12. Replace electrolytes • K+ is most important • Insulin shifts K+ into cells therefore K+ will fall as rehydrate • Consider adding K+ when serum K+ < 5.5 • Hyponatraemia may occur due to osmotic effect of glucose - it will correct with treatment of DKA

13. Key Changes • Fixed rate insulin infusion • 0.1 u/kg/hr • Even when near normoglycaemia attained • Monitoring of capillary beta-hydroxybutyrate • Diagnosis • Monitoring adequacy of treatment • Endpoint for completion of treatment

14. Monitoring • Monitor urine output and vital signs closely • catheterize • Repeat U&E, glucose, venous bicarbonate – ABG PAINFUL • 2 – 4 hours, 6 - 8 hours, 12 hours, 24 hours • Repeat ABG at 2 hours if not improving • ? Alternative cause for acidosis e.g. lactate

15. What should we be expecting? The hospital and home use of a 30-second hand-held blood ketone meter: guidelines for clinical practice T. M. Wallace, N. M. Meston*, S. G. Gardner² and D. R. Matthews Diabetic Medicine, Volume 18, Issue 8(p 640-645) • Wallace et al 2001 • Ketones on presentation 3.9 – 12.33 • Median half life of beta-hydroxybutyrate was 1.64 hrs • Suggested rate of ketone fall of 1 mmol/l/hr as indicator of adequate treatment

16. Suggestions • Review if glucose not improving by 3-5 mmol/L/h or ketones by 0.5 – 1 mmol/L/h • First check hydration has been addressed • Check infusion equipment • Lines • Pump • Solution • Increase rate of insulin infusion • Unclear by how much • Some sources say double • Guidelines say increase by 1-2u/h

17. Cause of Vomiting and Abdominal Pain • Vomiting • Excess ketone bodies causes vomiting • Gastric atony due to electrolyte imbalance • Abdominal pain • Peritoneal dehydration • Pancreatitits

18. What happens to the following in DKA? Plasma Total body Magnesium Phosphate Chloride Cholesterol Triglycerides Lipoprotein Amylase With treatment

19. Pitfalls • Does a high wcc mean infection? • No, not necessarily! • Give antibiotics as guided by findings • Absence of fever doesn’t mean absence of infection • Consider alternative cause for acidosisif glucose and acidosis markedly out of proportion • Non specific abdo pain and raised amylase doesn’t always mean pancreatitis • Do not stop insulin even if the blood glucose is normal or below 4

20. Discharge, Prognosis and Prevention • How do you stop a sliding scale? • Overlap with normal insulin (breakfast) and keep in for an other 24 hours to monitor BMs • Prevention • Diabetic nurse + docs can use opportunity for patient education about insulin regime etc. • Mortality is < 5% • Patients with frequent episodes are at increased risk of dying and diabetic complications

21. HHS/HONK • Hallmark of type 2 DM • May occur in: • New diagnosis • Poor compliance with treatment • Intercurrent illness – especially MI, Infection, CVA • Drugs- Steroids • Sugary drinks

22. Tissue glucose uptake glycogenolysis gluconeogenesis proteolysis lipolysis Hepatic glucose output Plasma free fatty acids Plasma amino acids hyperglycaemia Plasma osmolality ketogenesis Urea synthesis Glycosuria/ Osmotic diuresis thirst Loss of water Na & K + vomiting ketonaemia hypovolaemia hyperventilation acidosis Prerenal uraemia GFR Renal H+ excretion

23. Why is it different from DKA? • Insulin production markedly reduced but NOT absent. • No switch to fat metabolism and therefore no ketones or acidosis • Mortality markedly higher • Co-morbidities, longer time to diagnosis, electrolyte disturbances • Cerebral oedema and Pulmonary Embolism more common

24. How do I recognise it? • Diagnosis requires ALL of the following: • Raised blood glucose (usually >30mmol) • Absence of ketones (or + or ++ only) • Serum osmolality >350mmol

25. How do you calculate osmolality? 2(Na+K) + urea + glucose Or Ask for a serum level (U and E bottle, biochemistry)

26. Clinical features • Possibly osmotic symptoms • Dehydration around 10L deficit • decrease LOC • signs of underlying infection in upto 50% • +/- thrombo-embolism in up to30% • 2/3 cases previously undiagnosed • As high as 50% mortality

27. Is the treatment the same as DKA? • Fluid replacement – SLOWER (may be a marker of population not pathology) • Electrolyte replacement (pseudohyponatraemia) • Insulin – ‘slower’ scale • Search for cause • ANTICOAGULATION • Monitor

28. HYPOGLYCAEMIAzero tolerance • Definition:is a plasma glucose of<3mmol/l • Requires immediate treatment or Low blood glucose level with symptom complex or Requiring 3rd party rescue

29. Symptoms • Fall in glucose triggers fixed hierarchy of events: • 1) inhibition of insulin secretion • 2) release of glucagon and adrenaline (~3.8mmol/l) • 3) hypoglycaemic symptoms (~3.0mmol/l) All the above responses are diminished especially Glucagon Response

30. Symptoms • Autonomic • sweating, palpitations, tremor,hunger • Neuroglycopenia • confusion, clumsiness, behavioural changes • Non-specific • nausea,headache

31. Reactive Hypoglycaemia Post prandial gastric surgery Drug Induced insulin sulphonylureas alcohol Fasting P- pituitary failure L- liver disease A- Addison I - Islet cell tumours N- neoplasm- retroperitoneal fibro sarcomas Aetiology

32. Treatment of hypoglycaemia • If able to eat • glucose: e.g 3 dextrosol tabs / 200mls of orange juice/ coca cola • followed by long acting carbohydrate eg toast/ sandwich • In a semi-conscious patient • In the community: 1mg glucagon im and long acting carbohydrate on recovery

33. Severe Hypoglycaemia • Consider in any unconscious patient, those with CVA or odd behaviour • Hospital options- • I.M. glucagon 1mg • I.V. 20% [50%*] dextrose (typically 50 ml) • Other options- Hypostop gel • Look for precipitants/causes and avoid • Psychological consequences • Review oral hypoglycaemic drugs • Driving precautions and regaining awareness *Extravasation of 50% dextrose can cause severe tissue loss; 20% preferable

34. An example A 39 year old man is brought in by his wife. He is dehydrated and a little confused. He is not known to be diabetic but his BM on arrival is 25mmol.

35. Further information • Serum glucose 24 mmol • Urine ketones ++ • Blood gas - machine broken • Bicarbonate awaited Is this DKA or HONK? His wife is present. What questions might you ask her to help you work out what is going on?

36. Diagnosing Diabetes

37. Any questions about diabetic emergencies?