DKA - Notes
Posted: 18 Oct 2013, 05:04
Diabetic Ketoacidosis
In children under 10 years of age, diabetic ketoacidosis causes 70% of diabetes-related deaths. Diabetic ketoacidosis is defined by the triad of hyperglycemia, acidosis, and ketosis.
Clinical Presentation
Diabetes is newly diagnosed in 20% of cases of diabetic ketoacidosis. The remainder of cases occur in known diabetics in whom ketosis develops because of a precipitating factor, such as infection or noncompliance with insulin.
Symptoms of DKA include polyuria, polydipsia, fatigue, nausea, and vomiting, developing over 1 to 2 days. Abdominal pain is prominent in 25%.
Physical Exam
Patients are typically flushed, tachycardic, and tachypneic. Kussmaul's respiration, with deep breathing and air hunger, occurs when the serum pH is between 7.0 and 7.24.
A fruity odor on the breath indicates the presence of acetone, a by-product of diabetic ketoacidosis.
Fever is seldom present even though infection is common. Hypothermia and hypotension may also occur. Eighty percent of patients with diabetic ketoacidosis have altered mental status. Most are awake but ; 10% are comatose.
Laboratory Findings
Serum glucose level >250 mg/dL
pH <7.35
Bicarbonate level below normal with an elevated anion gap
Presence of ketones in the serum
Indications for Hospital Admission of Patients with Diabetic Ketoacidosis
Hyperglycemia (glucose >250 mg/dL)
Arterial pH <7.35, or venous pH <7.30, or serum bicarbonate <15 mEq/L
Ketonuria, ketonemia, or both
Differential Diagnosis
Differential Diagnosis of Ketosis-Causing Conditions
Alcoholic ketoacidosis does not cause an elevated serum glucose. Alcoholic ketoacidosis occurs with heavy drinking and vomiting.
Starvation ketosis occurs after 24 hours without food and is not usually with DKA because glucose and serum pH are normal.
Differential Diagnosis of Acidosis-Causing Conditions
Metabolic acidoses are divided into increased anion gap (>14 mEq/L) and normal anion gap (anion gap is determined by subtracting the sum of chloride plus bicarbonate from sodium).
Anion gap acidoses can be caused by any of the ketoacidoses, including DKA, lactic acidosis, uremia, salicylate or methanol poisoning.
Non-anion gap acidoses are associated with a normal glucose level and absent serum ketones. Non-anion gap acidoses are caused by renal or gastrointestinal electrolyte losses.
Hyperglycemia caused by hyperosmolar nonketotic coma occurs in patients with type II diabetes with severe hyperglycemia. Patients are usually elderly and have a precipitating illness. Glucose level is markedly elevated (>600 mg/dL), osmolarity is increased, and ketosis is minimal.
Treatment of Diabetic Ketoacidosis
Fluid Resuscitation
Fluid deficits average 5 liters or 50 mL/kg. Resuscitation consists of 1 liter of normal saline over the first hour and a second liter over the second and third hours. Thereafter, ½ normal saline should be infused at 250 mL/hr.
When the glucose level decreases to 250 mg/dL, 5% dextrose should be added to the replacement fluids to prevent hypoglycemia. If the glucose level declines rapidly, 10% dextrose should be infused, along with regular insulin, until the anion gap normalizes.
Insulin
Insulin is infused at 0.1 U/kg per hour. The biologic half life of IV insulin is less than 20 minutes. The insulin infusion should be increased each hour so that the glucose decline does not exceed 100 mg/dL per hour.
When the bicarbonate level is greater than 16 mEq/L and the anion gap is less than 16 mEq/L, the insulin infusion rate should be decreased by half.
Potassium
The most common preventable cause of death in patients with DKA is hypokalemia. The typical deficit is between 300 and 600 mEq.
Potassium chloride should be started when fluid therapy is started. In most patients, the initial rate of potassium replacement is 20 mEq/h, but hypokalemia requires more aggressive replacement (40 mEq/h).
All patients should receive potassium replacement, except for those with renal failure, no urine output, or an initial serum potassium level greater than 6.0 mEq/L.
Sodium
Patients with diabetic ketoacidosis sometimes have a low serum sodium level because the high level of glucose has a dilutional effect. For every 100 mg/dL that glucose is elevated, the sodium level should be assumed to be higher than the measured value by 1.6 mEq/L.
Frequently, patients have an initial serum sodium greater than 150 mEq/L, indicating severe dehydration. For these patients, initial rehydration fluid should consist of ½ normal saline.
Phosphate
Diabetic ketoacidosis depletes phosphate stores.
Serum phosphate level should be checked after 4 hours of treatment. If it is below 1.5 mg/dL, potassium phosphate should be added to the IV solution.
Bicarbonate therapy is not required unless the arterial pH value is 7.0 or lower. For a pH of <7.0, intravenous administration of 88 mEq/L of sodium bicarbonate is recommended.
Additional Therapies
A nasogastric tube should be inserted in semiconscious patients to protect against aspiration.
Deep vein thrombosis prophylaxis with subcutaneous heparin should be provided for patients who are elderly, unconscious, or severely hyperosmolar (5,000 U every 8 hours).
Monitoring of Therapy
Serum bicarbonate level and anion gap should be monitored to determine the effectiveness of insulin therapy.
Glucose levels should be check glucose level at 1-2 hour intervals during IV insulin administration.
Electrolyte levels should be assessed every 2 hours for the first 6-8 hours, and then q4h. Phosphorus and magnesium levels should be checked after 4 hours of treatment.
Plasma and urine ketones are helpful in diagnosing diabetic ketoacidosis, but are not necessary during therapy.
Determining the Underlying Cause
Infection is the underlying cause of diabetic ketoacidosis in 50% of cases. Infection of the urinary tract, respiratory tract, skin, sinuses, ears, or teeth should be sought. Fever is unusual in diabetic ketoacidosis and indicates infection when present. If infection is suspected, antibiotics should be promptly initiated.
Omission of insulin doses (common in adolescents) is often a precipitating factor.
Myocardial infarction, ischemic stroke, and abdominal catastrophes may precipitate DKA.
Initiation of Subcutaneous Insulin
When the serum bicarbonate level is normal and the patient is ready to eat, subcutaneous insulin can be started.
Intravenous and subcutaneous administration of insulin should overlap to avoid redevelopment of ketoacidosis. The intravenous infusion may be stopped 1 hour after the first subcutaneous injection insulin.
Estimation of Subcutaneous Insulin Requirements
Multiply the final insulin infusion rate times 24 hours. Two thirds of the total dose is given in the morning as two thirds NPH and one third regular insulin. The remaining one third of the total dose is given before supper as one half NPH and one half regular insulin. Subsequent doses should be adjusted according to the patient's
blood glucose response.
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A Journal of Clinical Emergency Medicine
January 2008
In children under 10 years of age, diabetic ketoacidosis causes 70% of diabetes-related deaths. Diabetic ketoacidosis is defined by the triad of hyperglycemia, acidosis, and ketosis.
Clinical Presentation
Diabetes is newly diagnosed in 20% of cases of diabetic ketoacidosis. The remainder of cases occur in known diabetics in whom ketosis develops because of a precipitating factor, such as infection or noncompliance with insulin.
Symptoms of DKA include polyuria, polydipsia, fatigue, nausea, and vomiting, developing over 1 to 2 days. Abdominal pain is prominent in 25%.
Physical Exam
Patients are typically flushed, tachycardic, and tachypneic. Kussmaul's respiration, with deep breathing and air hunger, occurs when the serum pH is between 7.0 and 7.24.
A fruity odor on the breath indicates the presence of acetone, a by-product of diabetic ketoacidosis.
Fever is seldom present even though infection is common. Hypothermia and hypotension may also occur. Eighty percent of patients with diabetic ketoacidosis have altered mental status. Most are awake but ; 10% are comatose.
Laboratory Findings
Serum glucose level >250 mg/dL
pH <7.35
Bicarbonate level below normal with an elevated anion gap
Presence of ketones in the serum
Indications for Hospital Admission of Patients with Diabetic Ketoacidosis
Hyperglycemia (glucose >250 mg/dL)
Arterial pH <7.35, or venous pH <7.30, or serum bicarbonate <15 mEq/L
Ketonuria, ketonemia, or both
Differential Diagnosis
Differential Diagnosis of Ketosis-Causing Conditions
Alcoholic ketoacidosis does not cause an elevated serum glucose. Alcoholic ketoacidosis occurs with heavy drinking and vomiting.
Starvation ketosis occurs after 24 hours without food and is not usually with DKA because glucose and serum pH are normal.
Differential Diagnosis of Acidosis-Causing Conditions
Metabolic acidoses are divided into increased anion gap (>14 mEq/L) and normal anion gap (anion gap is determined by subtracting the sum of chloride plus bicarbonate from sodium).
Anion gap acidoses can be caused by any of the ketoacidoses, including DKA, lactic acidosis, uremia, salicylate or methanol poisoning.
Non-anion gap acidoses are associated with a normal glucose level and absent serum ketones. Non-anion gap acidoses are caused by renal or gastrointestinal electrolyte losses.
Hyperglycemia caused by hyperosmolar nonketotic coma occurs in patients with type II diabetes with severe hyperglycemia. Patients are usually elderly and have a precipitating illness. Glucose level is markedly elevated (>600 mg/dL), osmolarity is increased, and ketosis is minimal.
Treatment of Diabetic Ketoacidosis
Fluid Resuscitation
Fluid deficits average 5 liters or 50 mL/kg. Resuscitation consists of 1 liter of normal saline over the first hour and a second liter over the second and third hours. Thereafter, ½ normal saline should be infused at 250 mL/hr.
When the glucose level decreases to 250 mg/dL, 5% dextrose should be added to the replacement fluids to prevent hypoglycemia. If the glucose level declines rapidly, 10% dextrose should be infused, along with regular insulin, until the anion gap normalizes.
Insulin
Insulin is infused at 0.1 U/kg per hour. The biologic half life of IV insulin is less than 20 minutes. The insulin infusion should be increased each hour so that the glucose decline does not exceed 100 mg/dL per hour.
When the bicarbonate level is greater than 16 mEq/L and the anion gap is less than 16 mEq/L, the insulin infusion rate should be decreased by half.
Potassium
The most common preventable cause of death in patients with DKA is hypokalemia. The typical deficit is between 300 and 600 mEq.
Potassium chloride should be started when fluid therapy is started. In most patients, the initial rate of potassium replacement is 20 mEq/h, but hypokalemia requires more aggressive replacement (40 mEq/h).
All patients should receive potassium replacement, except for those with renal failure, no urine output, or an initial serum potassium level greater than 6.0 mEq/L.
Sodium
Patients with diabetic ketoacidosis sometimes have a low serum sodium level because the high level of glucose has a dilutional effect. For every 100 mg/dL that glucose is elevated, the sodium level should be assumed to be higher than the measured value by 1.6 mEq/L.
Frequently, patients have an initial serum sodium greater than 150 mEq/L, indicating severe dehydration. For these patients, initial rehydration fluid should consist of ½ normal saline.
Phosphate
Diabetic ketoacidosis depletes phosphate stores.
Serum phosphate level should be checked after 4 hours of treatment. If it is below 1.5 mg/dL, potassium phosphate should be added to the IV solution.
Bicarbonate therapy is not required unless the arterial pH value is 7.0 or lower. For a pH of <7.0, intravenous administration of 88 mEq/L of sodium bicarbonate is recommended.
Additional Therapies
A nasogastric tube should be inserted in semiconscious patients to protect against aspiration.
Deep vein thrombosis prophylaxis with subcutaneous heparin should be provided for patients who are elderly, unconscious, or severely hyperosmolar (5,000 U every 8 hours).
Monitoring of Therapy
Serum bicarbonate level and anion gap should be monitored to determine the effectiveness of insulin therapy.
Glucose levels should be check glucose level at 1-2 hour intervals during IV insulin administration.
Electrolyte levels should be assessed every 2 hours for the first 6-8 hours, and then q4h. Phosphorus and magnesium levels should be checked after 4 hours of treatment.
Plasma and urine ketones are helpful in diagnosing diabetic ketoacidosis, but are not necessary during therapy.
Determining the Underlying Cause
Infection is the underlying cause of diabetic ketoacidosis in 50% of cases. Infection of the urinary tract, respiratory tract, skin, sinuses, ears, or teeth should be sought. Fever is unusual in diabetic ketoacidosis and indicates infection when present. If infection is suspected, antibiotics should be promptly initiated.
Omission of insulin doses (common in adolescents) is often a precipitating factor.
Myocardial infarction, ischemic stroke, and abdominal catastrophes may precipitate DKA.
Initiation of Subcutaneous Insulin
When the serum bicarbonate level is normal and the patient is ready to eat, subcutaneous insulin can be started.
Intravenous and subcutaneous administration of insulin should overlap to avoid redevelopment of ketoacidosis. The intravenous infusion may be stopped 1 hour after the first subcutaneous injection insulin.
Estimation of Subcutaneous Insulin Requirements
Multiply the final insulin infusion rate times 24 hours. Two thirds of the total dose is given in the morning as two thirds NPH and one third regular insulin. The remaining one third of the total dose is given before supper as one half NPH and one half regular insulin. Subsequent doses should be adjusted according to the patient's
blood glucose response.
-------------------------------------------------------------------------------------------------------------------------------------------------------
A Journal of Clinical Emergency Medicine
January 2008