تكفون اختصرو لي هالنص

1. Diagnosis


2. تكفون ابيكم تختصرو لي اللي فوق بنقطتين وكل نقطه ثلاثه سطور


3. Prognosis and Treatment


4. NOVOLIN


5. Drug Information


6. Drug Information


7. infusion of 0.1 unit/kg/h or higher with or without a bolus.


8. NOVOLIN


9. Drug Information

Diagnosis

In patients suspected of having DKA, serum electrolytes, BUN and creatinine, glucose, ketones, and osmolarity should be measured. Urine should be tested for ketones. Those who appear significantly ill and those with positive ketones should have ABG measurement. DKA is diagnosed by an arterial pH < 7.30 with an anion gap > 12 (see Sidebar 1: ) and serum ketones in the presence of hyperglycemia. A presumptive diagnosis can be made when urine glucose and ketones are strongly positive. Urine test strips and some assays for serum ketones may underestimate the degree of ketosis because they detect acetoacetic and not -hydroxybutyric acid, which is usually the predominant ketoacid.
Signs and symptoms of a triggering illness should be pursued with appropriate studies (eg, cultures, imaging studies). Adults should have an ECG to screen for acute MI and to help determine the significance of abnormalities in serum K.
Other laboratory abnormalities include hyponatremia, elevated serum creatinine, and elevated serum osmolarity. Hyperglycemia may cause dilutional hyponatremia, so measured serum Na is corrected by adding 1.6 mEq/L for each 100 mg/dL elevation of serum glucose over 100 mg/dL. To illustrate, for a patient with serum Na of 124 mEq/L and glucose of 600 mg/dL, add 1.6 (
/100) = 8 mEq/L to 124 for a corrected serum Na of 132 mEq/L. As acidosis is corrected, serum K drops. An initial K level < 4.5 mEq/L indicates marked K depletion and requires immediate K supplementation. Serum amylase and lipase are often elevated, even in the absence of pancreatitis (which may be present in alcoholic DKA patients and in those with coexisting hypertriglyceridemia

تكفون ابيكم تختصرو لي اللي فوق بنقطتين وكل نقطه ثلاثه سطور

Prognosis and Treatment

Mortality rates for DKA are between 1 and 10%. Shock or coma on admission indicates a worse prognosis. Main causes of death are circulatory collapse, hypokalemia, and infection. Among children with cerebral edema, 57% recover completely, 21% survive with n****logic sequelae, and 21% die.
The most urgent goals are rapid intravascular volume repletion, correction of hyperglycemia and acidosis, and prevention of hypokalemia. Identification of precipitating factors is also important. Treatment should occur in intensive care settings because clinical and laboratory assessments are initially needed every hour or every other hour with appropriate adjustments in treatment.
Intravascular volume should be restored rapidly to raise BP and ensure glomerular perfusion; once intravascular volume is restored, remaining total body water deficits are corrected more slowly, typically over about 24 h. Initial volume repletion in adults is typically achieved with rapid IV infusion of 1 to 3 L of 0.9% saline solution followed by saline infusions at 1 L/h or faster as needed to raise BP, correct hyperglycemia, and keep urine flow adequate. Adults with DKA typically need a minimum of 3 L of saline over the first 5 h. When BP is stable and urine flow adequate, normal saline is replaced by 0.45% saline. When plasma glucose falls to < 250 mg/dL, IV fluid should be changed to 5% dextrose in 0.45% saline.
For children, fluid deficits are estimated at 60 to 100 mL/kg body weight. Maintenance fluids (for ongoing losses) must also be provided (see Dehydration and Fluid Therapy: Maintenance requirements ). Initial fluid therapy should be 0.9% saline (20 mL/kg) over 1 to 2 h, followed by 0.45% saline once BP is stable and urine output adequate. The remaining fluid deficit should be replaced over 36 h, typically requiring a rate (including maintenance fluids) of about 2 to 4 mL/kg/h, depending on the degree of dehydration.
Hyperglycemia is corrected by administering regular insulin Some Trade Names
HUMULIN

NOVOLIN

Drug Information

0.15 unit/kg IV bolus initially, followed by continuous IV infusion of 0.1 unit/kg/h in 0.9% saline solution. Insulin should be withheld until serum K is 3.3 mEq/L (see Diabetes Mellitus and Disorders of Carbohydrate Metabolism: Treatment ). Insulin adsorption onto IV tubing can lead to inconsistent effects, which can be minimized by pre-flushing the IV tubing with insulin solution. If plasma glucose does not fall by 50 to 75 mg/dL in the first hour, insulin Some Trade Names
HUMULIN
NOVOLIN
Drug Information
doses should be doubled. Children should be given a continuous IV insulin Some Trade Names
HUMULIN
NOVOLIN

Drug Information

infusion of 0.1 unit/kg/h or higher with or without a bolus.

Ketones should begin to clear within hours if insulin is given in sufficient doses. However, clearance of ketones may appear to lag because of conversion of -hydroxybutyrate to acetoacetate (which is the “ketone” measured in most hospital laboratories) as acidosis resolves. Serum pH and HCO3 levels should also quickly improve, but restoration of a normal serum HCO3 level may take 24 h. Rapid correction of pH by HCO3 administration may be considered if pH remains < 7 after about an hour of initial fluid resuscitation, but HCO3 is associated with development of acute cerebral edema (primarily in children) and should not be used routinely. If used, only modest pH elevation should be attempted (target pH of about 7.1), with doses of 50 to 100 mEq over 30 to 60 min, followed by repeat measurement of arterial pH and serum K.
When plasma glucose becomes 250 to 300 mg/dL (13.88 to 16.65 mmol/L) in adults, 5% dextrose should be added to IV fluids to reduce the risk of hypoglycemia. Insulin dosage can then be reduced (minimum 1 to 2 units/h), but the continuous IV infusion of regular insulin should be maintained until the anion gap has narrowed and blood and urine are consistently negative for ketones. Insulin replacement may then be switched to regular insulin Some Trade Names
HUMULIN

NOVOLIN

Drug Information

5 to 10 units sc q 4 to 6 h. When the patient is stable and able to eat, a typical split-mixed or basal-bolus insulin regimen is begun. IV insulin should be continued for 1 to 4 h after the initial dose of sc insulin is given. Children should continue to receive 0.05 unit/kg/h insulin infusion until sc insulin is initiated and pH is > 7.3.
Hypokalemia prevention requires replacement of 20 to 30 mEq K in each liter of IV fluid to keep serum K between 4 and 5 mEq/L. If serum K is < 3.3 mEq/L, insulin should be withheld and K given at 40 mEq/h until serum K is 3.3 mEq/L; if serum K is > 5 mEq/L, K supplementation can be withheld. Initially normal or elevated serum K measurements may reflect shifts from intracellular stores in response to acidemia and belie the true K deficits that almost all DKA patients have. Insulin replacement rapidly shifts K into cells, so levels should be checked hourly or every other hour in the initial stages of treatment. Hypophosphatemia often develops during treatment of DKA, but phosphate repletion is of unclear benefit in most cases. If indicated (eg, if rhabdomyolysis, hemolysis, or n****logic deterioration occurs), K phosphate 1 to 2 mmol/kg of phosphate, can be infused over 6 to 12 h. If K phosphate is given, the serum Ca level usually decreases and should be monitored.
Treatment of suspected cerebral edema is hyperventilation, corticosteroids, and mannitol, but these are often ineffective after the onset of respiratory arrest
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