1 / 53

Diabetic emergencies –update and controversies

Dr. S. Parthasarathy MD., DA., DNB, MD ( Acu ), Dip. Diab . DCA, Dip. Software statistics PhD ( physio ) Mahatma Gandhi Medical college and research institute , puducherry India . Diabetic emergencies –update and controversies.

adrina
Télécharger la présentation

Diabetic emergencies –update and controversies

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab. DCA, Dip. Software statistics PhD (physio) Mahatma Gandhi Medical college and research institute , puducherry India Diabetic emergencies –update and controversies

  2. When ever there are updates , there will be controversies

  3. Diabetic emergencies • Diabetic keto acidosis • Hyper osmolar hyperglycemic non ketotic coma • Hypoglycemia • Lactic acidosis - ?? nonexistent

  4. Definition – clinical and biochemical • DKA is defined clinically as an acute state of severe uncontrolled diabetes associated with ketoacidosisthat requires emergency treatment with insulin and intravenous fluids • RBS = > 250 mg % • Ketones > 5 meq/l • pH < 7.3 bicarb < 18 meq / l

  5. Insulin Deficiency (Absolute or Relative) Glucose uptake Hepatic glucose Production Lipolysis Protein catabolism Glycerol Free Fatty acids Nitrogen loss Amino acids Ketogenesis Gluconeogenesis Hyperglycemia Ketonemia ELECTROLYTE DEPLETION Ketonuria Osmotic diuresis Hypotonic losses DEHYDRATION ACIDOSIS Pathophysiology of DKA

  6. Mind boggling slide !! Looks like As simple as this • Uncontrolled DM • Trigger factor • Severe hyperglycemia • Glycosuria , loss of water, electrolytes • Protein breakdown • Lipid breakdown and Ketogenesis

  7. What happens in DKA ?? • Hyperglycemia • Glycosuria • Water ( 6 litres) • Electrolytes ( K+ 300, Cl- 400 Na 500 meq) • Beta oxidation of fatty acids – • Keto acids • -acetone, beta-hydroxy butyrate, aceto acetate. • Fruity odour, nausea

  8. The “I” problem • I am the professor !! • I am rich !! • I am well qualified !! • I am the best doctor !! • I am the best husband !!

  9. The precipitating factors • Infection. • Infarction (heart or cerebrum) • Insulin lack. • Indiscrete drugs. • Infant (pregnancy) • Injuries • And as usual unidentified ??

  10. Update • avoid DKA • self-testing for urinary ketones and adjusting their insulin regimens on sick days.

  11. Symptoms Anorexia, Nausea, vomiting, Acute abdomen Lethargy, Myalgia, Dyspnea Hypothermia, Hyporeflexia, Hypotonia, Seizures , Stupor, coma Headache, chest pain, pleurisy

  12. Signs Air hunger – acidotic (kussmaul) respiration Dehydration,Confusion, drowsiness, coma (= 10%). Hypotension,Tachycardia Acetone odour on breath Any system

  13. We know medicine !! • symptom spectrum is a clinical collection but a patient may present with uncontrolled diabetes, an UTI and vomiting. • Beware don’t treat as gastritis. • It may be DKA • Uncontrolled diabetes , • Discomfort,vomiting • ECG – MI , Ketones + ve

  14. Diagnostic Criteria For DKA

  15. Take history !!

  16. Investigate • Blood – sugar , urea , creatinine, electrolytes • ABG, (venous BG) • ketones , TC, DC, blood cultures ,amylase, Serum lipase • CVP , X ray, • CT , MRI sos • ECG every 6 hours if doubted • Urine ketones, deposits and culture

  17. Plasma osmolarity • 2 (Na + K) + BUN/3 + glucose/18 • 2( 135 +5) + 15/3 + 300/18 • 280 + 5 + 16.6 = 301.6 • Around 290 in DKA • Around 310 in HHS

  18. Don’t believe lab fully • Test false • High glucose hyponatremia • High triglycerides low glucose • Ketones high creatinine

  19. Treat patients – not labs • Urine tests acetoacetate • But betahydroxy butyrate is predominant • Next day urine positive but patient better

  20. Treatment of DKA in Adults • Fluid replacement • Insulin replacement • Potassium replacement • Phosphate replacement • Bicarbonate replacement • Management of precipitating factor • General Medical Care (ICU).

  21. The average fluid deficit is 3–5 liters • In young, otherwise healthy patients • begin with bolus of 1 liter of normal saline • followed by an infusion of normal saline at 500 ml/hour for several hours.

  22. 1 +12 in medicine • IV fluids - Vary in infarct patients , • Appropriate monitoring and infusion √ • mild DKA should be given normal saline at 250 ml/hour; • those with elevated corrected serum sodium should be given half-normal saline at 250 ml/hour. (150 meq 0r osm 330 ) • Glucose NS at 250 mg or 180 mg • If sure of the electrolytes, Ringer lactate infusion is acceptable

  23. Insulin • loading dose of regular insulin at 0.1 units/kg • 60 kg means 6 units regular insulin IV • Followed by 6 units / hour • RBS comes down by 50 – 75 mg/ hour • RBS does not fall – double the dose • Mild cases no loading dose

  24. ActreActress jayamalasabarimala controversy • Insulin 0.14 units / kg start – no loading dose • IM regular insulin (0.3 units/kg), – some centers • Oral intake - SC insulin 6 hours prior to stopping IV • Extended insulin- better results

  25. Electrolyte replacement: • Serum potassium (mEq/L) Action • > 5.3 No additional potassium; recheck in 1 hr • 4.0–5.3 Add KCl 10 • 3.5 to < 4.0 Add KCl 20 • < 3.5 Hold insulin Add KCl 20–60 • Continuous cardiac monitoring

  26. Critically ill patients with DKA manifest hypophosphatemia during resuscitation • avoid potential cardiac and skeletal muscle weakness and respiratory depression from hypophosphatemia, a serum phosphate of < 1.5 mg/dl should be repleted with K2PO4 at 0.5 ml/hour. Usually rare

  27. NO ROUTINE bicarbonate • SIX’ indications of sodium bicarbonate after ABG • Arterial pH ≤ 7.0 • Serum HCO3 ≤ 5mmol/L • Imminent cardiovascular collapse /shock • Coma • Life threatening hyperkalemia • Severe lactic acidosis complicating DKA

  28. Laboratory tests follow up • Blood tests for glucose every 1-2 h until patient is stable, then every 6 h • Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h • Initial blood urea nitrogen (BUN) • Initial arterial blood gas (ABG) measurements, followed with bicarbonate as necessary

  29. Complications of DKA • The recovery pattern may be slow to come but complications like • cerebral oedema, arrhythmias stroke, infarction, aspiration, infection and sepsis may hinder the recovery to cause death in some patients. • Mortality (5-10%)

  30. Remember clinical clues • Monitor blood pressure, • pulse, respirations, • mental status, • fluid intake and output every 1–4 h.

  31. Update • DKA is a thrombotic state • DKA can precipitate stroke • Stroke can precipitate DKA

  32. DKA in pregnancy- points to note • with pregestational, insulin dependent diabetes • Foetal loss – 50 % • Maternal loss - 1 % • Proper antibiotic choice • Labour may precipitate DKA

  33. Paediatric DKA • 0.05 units /kg insulin • ideal to rehydrate in 36 hours than 24 fours • initial resuscitation with 20 ml/kg of 0.9 % NS • 0.45% saline avoids cerebral edema • SC lispro suggested

  34. Hyperglycemic hyperosmolar syndrome • Some insulin – no ketosis, no acidosis • Less common • Coma • Hyper osmolarity , • RBS 500- 600 • 10 liters or more Its is ideal to switch to half normal saline if either the osmolality or sodium is high. • No urgent insulin

  35. Hypoglycemia: • In practice, hypoglycemia is generally defined as a blood glucose level < 60 mg/dl. A definitive diagnosis • Whipple’s triad: • 1. Symptoms compatible with hypoglycaemia • 2. A low plasma glucose concentration • 3. Relief of symptoms after plasma glucose is raised.

  36. Why important • Brain needs glucose • It cant synthesize glucose • We cant let it starved of glucose for even a few minutes

  37. 40 or 50 or 60 or 70??? • Arterial plasma 10 % higher than venous. • Fasting ok but pp no good. • Whole blood (finger pricks) 10% lower!! • High hematocrit – venous-arterial gap is more.

  38. Incidence of hypo • Type 2 without insulin : 4-10 /patient/year • Type 2 on insulin : 16 /patient/year • Type 1 : 40 episodes /patient/year

  39. What happens if sugar decreases ?? • approx 80 mg • Decreased insulin secretion • Approx 70 mg • Increased glucagon • Approx 65 mg • Increased epinephrine • Approx 55-65 – • Cortisol & growth hormone (Noncritical) • Less than 55 - cognition affected

  40. Symptoms • Autonomicneuroglycopenic • Palpitation headache • Sweats fatigue • Anxiety mental dullness • Tremors vision blurring • Tachycardia confusion • Hypertension amnesia • Nausea ,hunger seizure,coma

  41. Risk factors • Use of insulin secretagogues ( sulphonylureas) • insulin therapy • Missed or irregular meals • Advanced age • Duration of diabetes, strict control • Impaired awareness of hypoglycemia • Autonomic failure, beta blockers DPP 4 inhibitors – less incidence

  42. In insulin patients !! • The depth of needle • Exercising limb • Hot bath after injection • Bigger size needle • Type of insulin • Glargine and detemir - less hypoglycemia

  43. Potentially hypoglycemic combines • Aspirin - dec. insulin resistance • Quinine – inc. insulin secretion. • Tetracyclics - inc. insulin secretion • Gatifloxacin - inc. insulin secretion • Beta blockers- interact hepatic gluconeo • Fibrates – sensitivity to insulin • Fluoxetine -stimulate beta cells • And a few others.

  44. Other diseases – prone for hypos • Adrenal • Gastrointestinal • Hepatic • Renal • Dementia • sepsis

  45. Categories of hypoglyemia • Mild : • 55-70 mg pallor,sweats,palpitation • Moderate : • 45-55 mg- headache,vertigo,mood changes • Severe : • < 45 mg. Conscious status?

  46. Treatment • Mild : 15 grams glucose = • increase 18 mg- 18 min • 4 cubes sugar • 2 spoons honey • 150 ml fruit juice

  47. Chocolate ,milk ,cereal bars – some sweets are not good Moderate: 20 -25 grams • Sulphonylureas induced • hypos – prolonged , • Observe and give snacks

  48. Severe – what is it?? • Patient needs someone’s help • 50 ml of 25 % dextrose IV –-------- • 2cc/kg-10% - infants • 2cc/kg – 25% - adolescents • 2cc/kg - 50% - adults • See that the vein is free flowing – • other wise risk of necrosis

  49. Some antidiabetics • Acarbose - alpha glucosidase inhibitor • So only glucose should be given • Miglitol -- sometimes even glucose may be refractory

  50. Treatment continuum • Measure blood sugar ,Assess conscious status • Maintain vitals, Start 10 % dextrose solution • 1 mg glucagon IM or SC • Look for precipitating factors-alcohol • Assess for liver status,renal status, • Serum insulin, c peptide, epinephrine, cortisol • TSH, growth hormones etc,etc…..

More Related