Understanding Hyperglycemic Crises: Diabetic Ketoacidosis (DKA) Management
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Diabetic Ketoacidosis
DKA is characterized by hyperglycemia (blood glucose more than 250 mg/dL, anion gap metabolic acidosis PH less than 7.3, and ketosis (positive urine and plasma ketones), along with dehydration and electrolyte abnormalities in varying degrees. Common ketone assays use nitroprusside, measuring acetoacetate and acetone, but not beta-hydroxybutyrate. presenting symptoms:
nausea/vomiting, abdominal pain, labored breathing (Kussmaul respirations), and polyuria. A mixed acid-base disorder may also be present, such as a concomitant severe contraction metabolic alkalosis elevating the serum bicarbonate level, masking the underlying metabolic acidosis.
Pathophysiology: In patients with DKA, the absolute lack of insulin causes an increase in counterregulatory hormones (cortisol, growth hormone, catecholamines, and glucagon), which promote lipolysis in adipose tissue and the release of free fatty acids. In the liver, the free fatty acids are converted to ketones. These patients suffer from a metabolic acidosis as a result of these circulating ketoacids. Ketone bodies contribute to the osmotic diuresis, and diuresis causes loss of sodium and potassium. Although initial laboratory values are variable, total body sodium and potassium are depleted.
Clinical features:
Presenting symptoms include polyuria, thirst, and altered mental state, ranging from lethargy to coma. Notably absent are symptoms of nausea, vomiting, and abdominal pain and the Kussmaul respirations characteristic of DKA. The prototypical pt is an elderly individual with a history of polyuria, weight loss, and diminished oral intake. In contrast to DKA, acidosis and ketonemia are usually not found; however, a small anion gap may be due to lactic acidosis, and moderate ketonuria may occur from starvation. Prerenal azotemia is typically present. Although the measured serum
sodium may be normal or slightly low, the corrected serum sodium is usually increased (add 1.6 meq to measured sodium for each 5.6-mmol/L [100-mg/dL] rise in the serum glucose). Even when adequately treated, has a significant mortality rate (up to 15%), which is in part explained by comorbidities and pt age.
Differential Diagnosis:
Alcoholic ketoacidosis
Uremia
Lactic acidosis
Sepsis
Management:
1. Initial Insulin Dosing & Administration
IV Bolus: 0.1–0.15U/kg regular insulin IV (use SC/IM only if no IV access).
Continuous IV Infusion: Standard mix is 100 U regular human insulin in 100 mL 0.9% NaCl (IV t1/2 = 5–9minutes.
DKA: Start at 0.1U/kg/hr
2. Blood Glucose (BG) Monitoring & Targets
Frequency: Check BG over 1hourly initially. Move to 2 hourly once stable (3 consecutive values within target decrease). Return to 1 hourly after any infusion rate change.
Target Drop Rate: 50–75\mg/dL/hr.
Dextrose Addition: Add Dextrose 5% to IV fluids when BG < 250 mg/dL.
Maintenance Goals:
Maintain BG at 150–200mg/dLuntil the anion gap closes.
3. Adjusting the Infusion Rate
BG drops too fast (>100 mg/dL/hr): Decrease IV insulin by 50%/hr.
BG drops too slow (<50 mg/dL/hr): Increase IV insulin by 50%/hr.
When BG reaches 250 mg/dL: The insulin infusion may need to be decreased by 50% to maintain target glucose levels.
4. Transition to Subcutaneous (SC) Insulin
Criteria to Start SC Insulin
DKA: Anion gap is closed AND serum bicarbonate is >15 mEq/L.
Patient must be able to eat.
Steps to Stop the Insulin Drip
Important: Do not stop the IV insulin drip until all of the following actions are completed:
Short-Acting Insulin: Give SC aspart or lispro at twice the hourly IV rate (e.g., if IV rate is 5 U/hr, give 10 U SC).
Long-Acting Insulin: Give SC NPH or glargine at 0.2–0.3U/kg.(divide 8 hourly if using NPH, or resume the patient's home dose.
Nutrition: Ensure the patient is served a meal and is actively eating.
*Lowering glucose >100 mg/dL/hr may cause osmotic encephalopathy.
**Failure to give SC insulin may result in rebound hyperglycemia and ketosis due to the short (half of Life )of IV regular insulin (5–9 min).
The precipitating problem should be sought and treated. Sufficient IV fluids (1–3 L of 0.9% normal saline over the first 2–3 h) should be given to stabilize the hemodynamic status. The calculated free water deficit (usually 9–10 L) should be reversed over the next 1–2 days, using 0.45% saline initially then 5% dextrose in water. Overly rapid fluid replacement should be avoided to prevent worsening of neurologic status. Potassium repletion is usually necessary. The plasma glucose may drop precipitously with hydration alone, though insulin therapy with an IV bolus of 0.1 units/kg followed by a constant infusion rate (0.1 units/ kg per hour) is usually required. If the serum glucose does not fall, the insulin infusion rate should be doubled. Glucose should be added to IV fluid when the plasma glucose falls to 11.1−13.9 mmol/L (200−250 mg/dL), and the insulin infusion rate should be decreased to 0.02–0.1 unit/kg per hour. The insulin infusion should be continued until the pt has resumed eating and can be transitioned to a subcutaneous insulin regimen.
Reference: The Washington Manual of Medical Therapeutics (Chapter 29); Diabetic ketoacidosis hyperosmolar hyperglycemic state by David A Rometo, Marin H, kollef, Garry s, Tobin, Harrison's Principles of Internal Medicine;Chapter 25 Diabetic ketoacidosis and hyperosmolar coma, CURRENT ESSENTIALS OF MEDICINEfourth edition by LAWRENCE M. TIERNEY, Jr. SANJAY SAINT ΜΑRY Α. WHOOLEY 181.
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