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Diabetes Emergencies

Diabetes Emergencies. Christian Hariman Christian.hariman@uhcw.nhs.uk. Today’s talk. Diabetes Ketoacidosis (DKA) Hyperosmolar Non Ketotic (HONK) Hypoglycaemia. Objectives. Recognise and participate in the management of diabetic ketoacidosis. Recognise Hyperosmolar Non ketotic state

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Diabetes Emergencies

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  1. Diabetes Emergencies Christian Hariman Christian.hariman@uhcw.nhs.uk

  2. Today’s talk • Diabetes Ketoacidosis (DKA) • Hyperosmolar Non Ketotic (HONK) • Hypoglycaemia

  3. Objectives • Recognise and participate in the management of diabetic ketoacidosis. • Recognise Hyperosmolar Non ketotic state • Recognise and manage hypoglycaemia.

  4. Case – Rose Smith • 18 year old girl, known diabetic type 1 • Brought in by her parents as she had been sick • Recently split from her boyfriend 2 days ago • Has been vomiting all night • She had been drinking alcohol with her mates yesterday to “cheer her up”

  5. How would you proceed? (1)

  6. How would you proceed? • ABC of resuscitation • History + examination • Pregnancy check? • Blood tests – FBC, U+E, LFTs, CRP, amylase • Blood glucose • Arterial blood gas • Urinary ketones

  7. A - patent • B - 29 breaths per minute, rapid shallow breaths, 100% on air • C – BP 102/68. Pulse 107. Cap refill 7 sec • History – as above • Examination – slightly tender abdomen • Pregnancy check –ve • Bloods taken • Peripheral blood glucose 9.0

  8. ABG • pH 7.20 • pO2 16.0 • pCO2 2.70 • HCO3- 13.8 • Na 140 • K 4.3 • Urinary ketones +ve

  9. What is your differentials + why? (2)

  10. What is your differentials + why? • Diabetes Ketoacidosis • pH, blood glucose (serum), ketones • Metabolic acidosis – other causes • Sepsis, poisoning • Pregnancy • Pancreatitis • Gastroenteritis

  11. Diabetes Ketoacidosis

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

  13. Loss of Beta cell function in pancreas Loss of beta cell function is gradual over time “Honeymoon period” alpha-cell beta-cell

  14. Symptoms and signs • Nausea • Vomiting • Abdominal pain • Often preceding polyuria, polydipsia, weight loss • Drowsiness/confusion/coma (severe) • Kussmaul respiration - hyperventilation • ‘Pear drops’ breath • Sign of associated systemic illness (MI, infection, etc)

  15. MUSCLE Diabetic Ketoacidosis:Pathophysiology Normal – glucose in blood B L O O D

  16. MUSCLE Diabetic Ketoacidosis:Pathophysiology Normal Mechanism B L O O D Insulin

  17. Liver Glucagon MUSCLE Diabetic Ketoacidosis:Pathophysiology • Insulin deficiency • *lack of glucose in muscle • glucagon excess • *increase in gluconeogenesis B L O O D Insulin

  18. MUSCLE Diabetic Ketoacidosis:Pathophysiology 3. Rapid lipolysis into free fatty acids and ketone bodies release of Beta-hydroxybutyrate ketones makes you sick B L O O D ketones ketones ketones ketones

  19. MUSCLE Diabetic Ketoacidosis:Pathophysiology 4. Hypovolaemia – vomitting + osmotic diuresis Increases concentration of ketones + glucose ketones B L O O D ketones

  20. How do I diagnose DKA? • Diagnosis requires all 3 of the following: • High blood sugar (i.e diabetes) Glucose > 11 mmol • *Finger-prick blood glucose can be normal* • Ketones (blood or urine ≥ +++) • Acidosis (pH<7.30 or HCO3<15mmol)

  21. How do I Manage DKA? • ABC – if impaired – consider early ITU input / central venous access • Replace fluids • Resolution of ketonaemia / insulin • Replace electrolytes • Look for cause • Close monitoring • Consider Low molecular weight heparin

  22. Replacing fluids Initial management • 1L 0.9% NaCl • 30 mins* • 1hr • 2hr • 4 hr Then continue NaCl 0.9% as dictated by fluid status *beware of elderly patients Later • Once blood glucose <14 mmol/L – give 10% dextrose alongside 0.9% Normal Saline at 125ml / hour

  23. Resolution of ketonaemiaInsulin infusion • Insulin infusion • 50units actrapid made to 50ml with NaCl 0.9% • Rate: 0.1 units/kg/hour • 70kg = 7 units/hour • Aim for fall in serum ketone of 0.5 mmol/L per hour • OR rise in serum HCO3- by 3 mmol/hr or reduction of Blood glucose by 3 mmol/hr • Increase rate of insulin by 1 unit per hour if above not achieved • Continue infusion until blood ketones <0.3, venous pH >7.3 and/or HCO3- >18

  24. Replace electrolytes • K+ is most important • Insulin shifts K+ into cells therefore K+ will fall as rehydrate • Serum K+ ≥ 5.5 • No potassium supplement • Serum K+ 3.5 - 5.4 • Add 20mmol per litre • Serum K+ <3.5 • Add 40mmol per litre • Hyponatraemia may occur due to osmotic effect of glucose - it will correct with treatment of DKA

  25. 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

  26. 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

  27. 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

  28. Hyperosmolar Non-Ketotic Hyperglycaemic State (HONK/HHS)

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

  30. MUSCLE HONK:Pathophysiology • Insulin production markedly reduced but NOT absent. • No switch to fat metabolism and therefore no ketones or acidosis • Gluconeogenesis • Loss of intravascular volume B L O O D Insulin

  31. Importance • Mortality markedly higher compared to DKA • Co-morbidities, longer time to diagnosis, electrolyte disturbances • Cerebral oedema and Pulmonary Embolism more common

  32. Clinical Presentation • Possibly osmotic symptoms • Dehydration around 10L deficit • Decreased level of conciousness • Signs of underlying infection in up to 50% • +/- thrombo-embolism in up to30% • 2/3 cases previously undiagnosed • As high as 50% mortality

  33. 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

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

  35. Is the treatment the same as DKA? • 1L 0.9% NaCl • 1 hr* • 2 hr • 4 hr • 8 hr Then continue NaCl 0.9% as dictated by fluid status *half the rate of DKA • Fluid replacement – SLOWER (may be a marker of population not pathology) • Electrolyte replacement (pseudohyponatraemia) • Insulin – ‘slower’ scale – normally very responsive to IV insulin • Search for cause • ANTICOAGULATION • Monitor

  36. Insulin • 50units actrapid made to 50ml with NaCl 0.9% • Rate: 0.1 units/kg/hour • 70kg = 7 units/hour • More insulin sensitive • Reduce rate if Blood glucose falls >10 mmol / hour • Consider halving the rate within the first 1-2 hours • Stop when patient is recovered

  37. Hypoglycaemia

  38. Hypoglycaemia • In diabetes: blood sugar < 4 mmol/l • Symptoms may not present at the same level of blood glucose • Autonomic: • sweating, palpitations, tremor, hunger • Neuroglycopenic • confusion, clumsiness, behavioural changes, seizures • Non-specific • nausea, headache, tiredness

  39. Causes • Drug Induced • insulin • sulphonylureas • Alcohol • Reactive Hypoglycaemia • Post prandial • gastric surgery

  40. 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 the community: 1mg glucagon im and long acting carbohydrate on recovery • Hospital options- • I.M. glucagon 1mg • I.V. 20ml of 50% dextrose* • Other: hypostop *Extravasation of 50% dextrose can cause severe tissue loss; 20% preferable

  41. Any questions about diabetic emergencies?

  42. Summary • You should be able to: • Recognise diabetic ketoacidosis. • Participate in the management of diabetic ketoacidosis. • Recognise Hyperosmolar Non ketotic state • Recognise and manage hypoglycaemia. • Christian.Hariman@uhcw.nhs.uk

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