A 60-year-old woman is admitted to the emerge-ncy department with evidence of spreading perito-nitis. Her temperature is 40°C with a pulse rate of 120/min and blood pressure of 96/60. Her blood sugar is 960 mg%. Urine specific gravity is 1.030, and marked glucosuria and ketonuria are present. The most important first step in her management is
|A||Administration of broad-spectrum antibiotics intravenously|
|B||Correction of hyperglycemia|
|C||Correction of ketoacidosis|
|D||Immediate diagnostic celiotomy|
a. DKA results from relative or absolute insulin deficiency combined with counter regulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormonE.. Both insulin deficiency and glucagon excess, in particular, are necessary for DKA to develop.
b. The decreased ratio of insulin to glucagon promotes gluconeogenesis, glycogenolysis, and ketone body formation in the liver, as well as increases in substrate delivery from fat and muscle (free fatty acids, amino acids) to the liver.
c. DKA is initiated by inadequate levels of plasma insulin.
d. Most commonly, DKA is precipitated by increased insulin requirements, as might occur during a concurrent illness. Failure to augment insulin therapy often compounds the problem.
e. Occasionally, complete omission of insulin by the patient or health care team (in a hospitalized patient with type 1 DM) precipitates DKA.
f. Patients using insulin infusion devices with short-acting insulin are at increased risk of DKA, since even a brief interruption in insulin delivery (e.g., mechanical malfunction) quickly leads to insulin deficiency.