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DKA

DKA. Presented by Dr Moosally Prepared by Mick Svoboda. epidemiology. Occurs primarily in type 1 diabetics but is also prevalent in type 2 Is the initial presentation of new onset DM in 20-30% of cases Accts for 24% of DM hsopital admissions. Pathophysiology.

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DKA

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  1. DKA Presented by Dr MoosallyPrepared by Mick Svoboda

  2. epidemiology • Occurs primarily in type 1 diabetics but is also prevalent in type 2 • Is the initial presentation of new onset DM in 20-30% of cases • Accts for 24% of DM hsopital admissions

  3. Pathophysiology • Insulin deficiency and counterregulatory hormone (glucagon, growth hormone, catecholamines, and cortisol) excess. • This causes hyperglycemia w/ the end result of → • osmotic diuresis • prerenal azotmemia • ketone formation • Wide anion gap acidosis

  4. DKA in pregnancy • Factors that increase risk of DKA in pregnant pts • Lower fasting serum glucose level→ relative insulin def. and increased baseline fatty acid levels • Increased counterregulatory hormones • Chronic resp. alkalosis → decreased bicarb levels • Increased episodes of vomiting and infections

  5. Etiology of DKA • Noncompliance of insulin therapy • Infection • MI • CVA • Trauma • PE • Surgery • Pancreatitis • Steroid use

  6. Clinical features • Clinical manifestations directly related to the primary metabolic derangements. • Hyperglycemia – results in the second metabolic abnormality, volume loss. • Volume loss – manifested by tachycardia, orthostasis or hypotension, poor skin turgor. • Acidosis – manifested by augmented ventilation, Kussmaul respiration. • Pts will often complain of n/v and abd pain.

  7. Ancillary tests • Bedside glucose - may be checked q 1hr to monitor therapy response. • EKG – most common finding sinus tach., watch for possible ischemia or hyper/hypokalemic changes • ABG vs. venous blood gas • Serum electrolytes – may be checked q 1-2 hrs to monitor therapy response. • Calculation of anion gap • Serum acetone • Lipase – more sensitive for underlying pacreatitis than amylase • Cardiac enz. - For suspected MI • CBC – elevated H/H and leukocytosis may reflect hemoconcetration

  8. Differential Diagnosis of DKA • Diag requires • Glucose > 250mg/dL • Bicarb < 15 mEq/L • pH < 7.30 • Differential • Alcoholic and starvation ketosis – milder ketosis w/ lower glucose levels compared to DKA • Uremia • Lactic acidosis • Ingestion – salicylates, ethylene glycol, methanol

  9. Treatment • Therapy starts with aggressive fluid resuscitation. • Additionally the pt should receive • Cardiac monitoring • Preferably 2 large bore IV lines • Antiemetics if nauseated • Urine output monitoring

  10. Fluid Administration • NS preferred initially • First liter – rapid over 30 mins • Second liter can go in at 500ml/hr • Additional fluid will be replaced but at slower rates • Fluid should be changed to D51/2NS once the serum glucose is 250-300 mg/dL if ketosis has not resolved

  11. Insulin therapy • Continuous IV infusion at low doses (0.1units/kg/hr) is preferred. • IV is more effective than SubQ if pt is vol. depleted 2˚ to decreased absorption. • Loading dose not proven to be beneficial and is not recommended in children. • Optional in adults (0.15units/kg) • Nonresponce rate of insulin is 1-2% and most often 2˚ to infection. • Insulin therapy should continue until anion gap clears

  12. Potassium • Total body deficiency 2˚ to insulin deficiency, acidosis, osmotic diuresis, and vomiting. • Recommendations for replacement • K+ > 3.3mEq/L but > 5.0mEq/L • Can add 10mEq of KCl per hour in the IVF for at least 4 hrs. • K+ > 5.0mEq/L • Avoid replacing K+ • K+ < 3.3mEq/L • Add 15-20mEq/L/h holding insulin for 30 min.

  13. Phosphate and Magnesium • Hypophsophatemia/magnesemia both created by extracellular shift and osmotic diuresis. • No clinical trial has demonstrated benefit from routine phosphate and magnesium therapy in the ED.

  14. Bicarbonate • No studies show improved clinical outcome w/ adding bicarb in tx of DKA • Disadvantages of bicarb administration • Hypokalemia • CNS acidosis • Cerebral edema • Hypertonicity and sodium overload

  15. Complications related to therapy • Hypoglycemia • Hypokalemia • Hypophosphatemia • ARDS • Cerebral edema • These complications can be minimized by a gradual return to normal metabolic balance.

  16. Disposition • The majority of pts in DKA will require hospital admission to a monitored bed setting.

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