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DKA & HHS

DKA & HHS. Ahmad F. Mady MD. Diabetes. 1552 BC , Diabetes 1st Described In Writing on 3 rd Dynasty Eqyptian papyrus by physician Hesy-Ra: mentions polyuria as a symptom.

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DKA & HHS

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  1. DKA & HHS Ahmad F. Mady MD

  2. Diabetes • 1552 BC, Diabetes 1st Described In Writing on 3rd Dynasty Eqyptian papyrus by physician Hesy-Ra: mentions polyuria as a symptom. • 250 BC, Apollonius of Memphis coined the name "diabetes” meaning "to go through" or siphon. He understood that the disease drained more fluid than a person could consume.

  3. Diabetes Mellitus • Gradually the Latin word for honey, "mellitus," was added to diabetes because it made the urine sweet. • Up to 11th century diabetes was commonly diagnosed by “water tasters” who drank the urine of those suspected of having diabetes, as it was sweet-tasting.

  4. Early Diabetes Discoveries • In the 1869, Paul Langerhans, a German medical student announced in a thesis, that the pancreas contains two systems of cells. • In the1889 Oskar Minkowski and Joseph von Mering in France, removed the pancreas from a dog to determine the effect of an absent pancreas on digestion

  5. Fredrick Banting & Charles Best

  6. Leonard Thompson

  7. Three months later

  8. Ppt Factors of DKA&HHS

  9. Clinical Presentation of DKA • History of polyuria, polydipsia, polyphagia, weight loss • Nausea, vomiting, abdominal pain • Acidemia leading to hyperventilation,Kussmaul breathing,Ketotic odour. • Clouding of sensorium, weakness, and coma • Dehydration and shock

  10. Clinical Presentation of HHS • Similar to DKA but coma is more frequent • Severe dehydration is the rule • Focal neurologic deficits may be found at presentation • Usually more elderly patients • Acidemia not pronounced

  11. Laboratory Findings

  12. Therapeutic goals Treatment involves 5 key components: • Monitoring • Fluid resuscitation • Insulin and dextrose infusion • Electrolyte repletion • Treating underlying cause

  13. Dehydration WHY……?

  14. Fluids, fluids, fluids! • Restores circulatory volume • Diminish concentration of catecholamines, glucagon

  15. Caution! • Excessive therapy may result in ARDS • Cerebral edema • Hyperchloremic acidosis

  16. Fluid replacement in DKA • Initial fluid = normal saline • 15ml to 20ml/kg, about 1-2L in 1 hour • 500 ml/h for next 2 hours or 1L /h if in shock • 500-250 ml/h according to hydration status (RBS 250mg/dl) • Subsequent change in fluids • half normal saline • START when urine output improves and BP stable • D5 1/2 NS • START when blood glucose <250 mg/dl • Endpoint - resolution of ketonemia and acidosis - Se bicarbonate >18

  17. Fluid replacement in HHS • If SBP<90 mmHg • Initially give 1 litre of Normal Saline per hour. • If SBP>90 mmHg • 0.45% N/S if serum sodium is high or normal • 0.9% N/S if serum sodium is low. • Rate and volume as for DKA. • Rate should be adjusted for cardiac function

  18. Insulin administration in DKA&HHS • Withhold insulin therapy until the serum potassium concentration has been determined. • Initial regular insulin • Goal = reduce hourly glucose by 50-70 mg/dl • Bolus = 0.15u/kg or 10u bolus • IV infusion = 0.1u/kg/hr till RBS 250mg/dl then follow iv infusion protocol

  19. Insulin administration in DKA&HHS • Endpoint for continuous/hourly regular insulin • Se bicarbonate >18, anion gap <14 • Absence of serum ketones • Switch over to maintenance Plasma glucose is less than 250 mg/dl DKA has resolved Patient is tolerating PO • It is important to give the first s.c. injection of insulin approximately 2 hours before stopping the i.v. route

  20. Intravenous Insulin Infusion Protocol

  21. Who saved me: the insulin or the nurse ?

  22. Potassium Therapy may be normal or elevated at the time of diagnosis Goal is to maintain Se K between 4 and 5 • If serum K>5 do not give K but recheck in one hour • If serum K is 4-5 give KCl 20 mEq in each litre of fluid • If serum K is 3-4 give KCl 30 mEq in each litre of fluid • If serum K is <3 hold insuline,give KCl 40 mEq over 1hr then recheck K

  23. Bicarbonate Therapy • Controversial • Most literature shows no benefit to using bicarbonate with patients who have DKAor HHS • No differences in reduction of glucose or ketoanion • May increase hypokalemia, cerebral acidosis and cardiac dysfunction • For patients with pH < 7.0, they may benefit from bicarbonate therapy • pH 6.9-7.0 may give 50 mEq of bicarb • pH <6.9, may give 100 mEq of bicarb

  24. Phosphate Therapy • Phosphate deficiency – Osmotic diuresis → urinary phosphate losses – Insulin therapy → serum phosphate reenters intracellular compartment • Adverse complications may occur if P < 1.0 mg/dl • Respiratory depression • Skeletal muscle weakness • Hemolytic anema • Cardiac dysfunction • May be useful to replace 1/3 potassium as K3PO4, reduce chloride load, prevent hyperchloremic acidosis.

  25. Investigations to be done • Serum glucose initially then hourly • Serum K initially then hourly if <3 or >5 otherwise 2 hourly till stable • Na, urea, creatinine initially then 4 hourly till stable • ABG initially then as often as necessary • Serum osmolality & Na hourly initially in HHS • CBC with differential white count • ECG, CXR • Urine analysis • Urine culture if pus cells or bacteria in U/A or patient is septic • Blood culture if patient is febrile or WBC>12,000 • Serum Mg and Ca • Cardiac enzymes if ECG abnormal initially and after 8 hours • Throat swab culture if signs of pharyngitis present • Sputum culture if purulent looking or infiltrate on CXR • Serum amylase (often raised-up to 10 times-even in the absence of pancreatitis)

  26. Considerations in management • Avoid overhydration • Note: Nitroprusside can be used to detect ketones but is not accurate ….why? • Prophylaxis small doses of LMW heparin • Antibiotics: NOT routine • Do consider anti-peptic ulcer prophylaxis

  27. Complications • Lactic acidosis – Due to prolonged dehydration, shock, infection and tissue hypoxia – Should be suspected in pt with refractory metabolic acidosis and persistent anion gap • Arterial thrombosis – Stroke, MI, or an ischemic limb • Cerebral edema – Over hydration of free water, excessively rapid correction of hyperglycemia are risk factors • ARDS – Excessive crystalloid infusion – Pulmonary rales, increased AaO2 gradient

  28. Mortality from DKA is due to? 1) Hyperglycemia 2) Acidosis 3) Sepsis 4) Hypokalemia 5) Cerebral edema

  29. Protocol DKA

  30. Three Take Home Messages • DKA &HHS may be life threatening • Fluids and Insulin along with frequent monitoring is essential • Watch for hypokalemia and cerebral edema

  31. Thank you for your attention Thank you for saving me from DKA&HHS

  32. Thank you AHMADF. MADY MD

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