Hassan Mohammad AlShehri

ID#2051040006

Diabetic Ketoacidosis
:Pathogenesis Alterations in metabolism Hyperglycemia results from Increased gluconeogenesis Conversion of glycogen to glucose Inadequate use of glucose by peripheral tissues Ketone bodies result from Beta oxidation of FFA (increased liberation of free fatty acids due to the loss (of the inhibitory action of insulin on the hormone sensitive lipase (Decreased concentrations of malonyl coA (an inhibitor of ketogenesis :Precepitating factors Infection Inadequate use of insulin New onset diabetes Medical, surgical or emotional stress Drugs: Corticosterioids, thiazide diuretics Pancreatitis Clinical presentation anorexia, N/V, along with polydepsia and polyuria for about 24 hrs. followed by stupor or coma Abdominal pain and tenderness could be present ”Kussmaul breathing with fruity odor “acetone (Sings of dehydration (HR increase, postural hypotension Diagnostic criteria for DKA hyperglycemia >250 mg/dl ketosis (ketonemia or ketonuria acidosis pH<7.3, HCO3<15mEq/L supporting features are volume depletion and Kussmaul’s breathing Severity: Mild Moderate Atrial pH 7.25-7.3 7.00-<7.24 Serum HCO3 15-18 10-<15 Anion gap >10 >12 Mental status alert alert/drowsy anion gap : Na -(Cl + HCO3) = 12 Sever <7.00 <10 >12 stuper/coma

:Managment :Goals of treatment of DKA • intravascular volume expansion • Decrease serum glucose • Clear serum of ketoacids and reach pH>7.3 • Correct electrolyte imbalances Fluids: The initial fluid of choice is isotonic saline, which is recommend to be infused at the rate of 15–20 ml /kg body weight per hour or 1–1.5 L during the first hour. The goal is to replace half of the estimated water deficit over a period of 12- 24 hours Insulin: IV bolus of regular insulin (0.1 U/kg body weight) and continuous infusion of regular insulin at the dose of 0.1U/kg/hr as the method of choice. The optimal rate of glucose reduction would be between 50- 70 mg/hr. If it is not achieved in the first hour, the insulin dose may be doubled continue insulin administration until ketonemia is controlled when plasma glucose reaches 200 mg/dl, the hydration fluid should be changed to D5 ½ NS, and insulin rate should be decreased to 0.05 U/kg/hr. The rate of insulin should be adjusted to maintain blood glucose between 150-200 Pottasium: Total body K is low even if plasma report is high. Mild to moderate hyperkalemia is frequently seen in patients with DKA, due to acidosis, proteolysis and insulinopenia Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentrations Potassium replacement is initiated after serum levels fall below 5.3 mEq/l, in patients with adequate urine output (50 ml/h). Adding 20–30 mEq potassium to each liter of infused fluid is sufficient to maintain a serum potassium concentration within the normal range of 4–5 mEq/L Do not give K in first hour unless K < 3.5 HCO3: Consider NaHCO3 if pH < 7.0 stop the infusion at pH 7.2 to avoid alkalosis upon reversal of ketosis associated with some adverse effects, such as hypokalemia , decreased tissue oxygen uptake and cerebral edema and delay in the resolution of ketosis

DKA resolution: blood glucose is < 200 mg/dl, serum bicarbonate is > 18, pH is > 7.30 anion gap is < 12 :Subcutaneous insulin initiation Begin as soon as patient is fit to eat Inject at least 30 min before stopping IV insulin ways begin with regular or short-acting analogue Complications of DKA manegment • Hypoglycemia • Hypokalemia • Cerebral odema. • Hypoxemia and non cardiogenic pulmonary odema. • Thrombosis

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