eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care
Diabetic Ketoacidosis: Treatment & Medication
Updated: Dec 11, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
As always, in patients with diabetic ketoacidosis (DKA), the first principals of resuscitation apply (ie, ABCs).1 Outcomes are best when children are closely monitored and changing status is promptly addressed.30,31 Give oxygen, although this has no effect on the respiratory drive of acidosis. Diagnose by clinical history, physical signs, and elevated blood glucose.
- Fluid replacement: No randomized trials of fluid replacement have been conducted, and over the years, various regimens have been proposed. Published series suggest the best outcomes have been achieved by using isotonic sodium chloride solution or half-strength sodium chloride solution for first resuscitation and replacement.31 Slowly correcting the fluid deficit over 24-48 hours appears safer than rapid rehydration and, thus, forms the basis for the regimen that follows:
- Calculate fluid deficit by weight loss or clinical assessment to a maximum 10% of body weight.
- In a child with severe acidosis or compromised circulation, an initial resuscitation of 10-20 mL/kg of isotonic sodium chloride solution (0.9%) can be administered over 30 minutes.
- After resuscitation, slowly correct the fluid deficit over 48 hours by providing normal maintenance fluids together with the calculated deficit.
- Remember to include any fluid bolus in the total volume of fluid to be replaced.
- Administer isotonic sodium chloride solution until blood glucose levels have fallen to 250-300 mg/dL (ie, 12-15 mmol/L), at which time glucose-containing fluids should be introduced (either 5% glucose with 0.9% saline or 5% glucose with 0.45% saline). Continue maintenance with dextrose saline until the child is eating and drinking normally.
- If cerebral edema develops, restrict fluid replacement to two thirds of normal maintenance and replace the deficit over 48 or more hours.
- Although strict assessment of fluid balance is important, replacement of ongoing losses is not normally required.
- Insulin replacement
- Continuous, low-dose intravenous (IV) insulin infusion is generally accepted as the safest and most effective method of insulin delivery for treating diabetic ketoacidosis. Low-dose IV insulin infusion is simple, provides more physiological serum levels of insulin, allows gradual correction of hyperglycemia, and reduces the likelihood of sudden hypoglycemia and hypokalemia.
- The results of a prospective national study of diabetic ketoacidosis in the United Kingdom suggest a greater risk of cerebral edema in patients who received insulin within the first hour of treatment.7 In light of these results, starting insulin therapy an hour after fluid resuscitation has commenced is prudent, especially in the newly diagnosed child.
- The correct dose of insulin to infuse in the treatment of diabetic ketoacidosis is under debate. Traditionally, 0.1 U/kg/h is given, but a lower dose of 0.05 U/kg/h is enough to prevent gluconeogenesis and results in a slower reduction of blood glucose levels. Regularly reviewing the response to treatment and adjusting rates accordingly is probably better than having a single fixed rate. Adolescents with secondary DKA and insulin resistance may need more than 0.1 U/kg/h.
- Authorities commonly recommend that blood glucose levels not fall faster than 90 mg% (ie, 5 mmol/L) per hour. The infusion rate of insulin can be reduced as blood glucose levels fall but should not drop below 0.05 U/kg/h to prevent any recurrence of ketosis. Do not discontinue infusion until subcutaneous (SC) insulin has been given when the child has recovered. If blood glucose falls below 120 mg% (ie, 7 mmol/L), increase the concentration of infused glucose to prevent hypoglycemia. Ketosis clears more quickly if insulin infusions are prolonged for 36 hours or more.
- In cases of mild-to-moderate diabetic ketoacidosis where the patient is able to tolerate oral fluids, giving repeated (hourly) SC injections of regular or fast-acting analogue insulins in a dose of 0.1U/kg is possible. This is as effective as intravenous insulin.32,33
- Electrolyte replacement
- Potassium: Patients with DKA always have a total body deficit of potassium. After initial resuscitation and if serum/plasma levels are below 5 mEq/L or a good renal output has been maintained, add potassium to all replacement fluids. Table 2 provides examples of infusion concentrations as mEq/L for differing degrees of potassium status. Potassium chloride most commonly is administered. This theoretically could make the acidosis worse, but no evidence indicates that administration of other potassium salts such as phosphate or acetate is more effective.
- Table 2. Infusion Rates of Potassium Chloride
Open table in new window
[ CLOSE WINDOW ]Table
Serum/Plasma K+ (mEq/L) Potassium Chloride (KCL) Dose in Infusion Fluids <2.5 mEq/L Carefully monitored administration of 1 mEq/kg body weight by separate infusion over 1 h 2.5-3.5 mEq/L 40 mEq/L 3.5-5 mEq/L 20 mEq/L 5-6 mEq/L 10 mEq/L (optional) Over 6 mEq/L Stop K+ and repeat level in 2 h Serum/Plasma K+ (mEq/L) Potassium Chloride (KCL) Dose in Infusion Fluids <2.5 mEq/L Carefully monitored administration of 1 mEq/kg body weight by separate infusion over 1 h 2.5-3.5 mEq/L 40 mEq/L 3.5-5 mEq/L 20 mEq/L 5-6 mEq/L 10 mEq/L (optional) Over 6 mEq/L Stop K+ and repeat level in 2 h - Bicarbonate: Although metabolic acidosis may be severe, no evidence supports administration of IV sodium bicarbonate to improve outcomes; on the contrary, the evidence indicates that IV bicarbonate may cause harm and delay recovery.34,35 Failure of the acidosis to improve with treatment more likely reflects inadequate fluid and insulin replacement. The only justification for using IV bicarbonate is acidosis sufficiently severe to compromise cardiac contractility.
- Other electrolytes: Although patients usually have an absolute deficit of phosphate and magnesium, no evidence indicates that either needs to be replaced in patients with diabetic ketoacidosis.
- Regular assessment
- Attention to detail is important to achieving a good outcome. Specifically designed recording charts (see Media files 4-7) make the process of care much easier. Ideally, these charts include all important measurements of clinical and biochemical status, fluid balance, and insulin prescription.
- Frequent review of neurologic status, at least hourly (or any time a change in level of consciousness is suspected), is essential during the first 12 hours of diabetic ketoacidosis treatment. Promptly treat any suspected cerebral edema.
Consultations
- Consult a neurosurgeon if cerebral edema is suspected.
Diet
- Once the child has recovered, he or she can resume a normal diet.
Medication
The cornerstones of diabetic ketoacidosis (DKA) management are fluid resuscitation, insulin administration, electrolyte monitoring and administration, and close observation to minimize the effect of cerebral edema.
Fluid replacement
The best outcomes have been achieved by using normal or half-strength saline (ie, 0.9% or 0.45% sodium chloride) for first resuscitation and replacement. Slowly correcting the fluid deficit over 24-48 h appears safer than rapid rehydration.
In a child with severe acidosis or compromised circulation, an initial resuscitation of 10-20 mL/kg of isotonic sodium chloride solution (0.9% NaCl) can be administered over 30 minutes. After resuscitation, slowly correct the fluid deficit over 24-48 h by providing normal maintenance fluids together with the calculated deficit. Administer isotonic sodium chloride solution until blood glucose levels have fallen to 250-300 mg/dL (ie, 12-15 mmol/L), at which time glucose-containing fluids should be introduced (eg, 5% glucose with 0.45% NaCl). Continue maintenance with dextrose saline until the child is eating and drinking normally.
Sodium chloride 0.9% (Normal Saline)
Used for resuscitation and dehydration associated with DKA. Calculate fluid deficit by weight loss or clinical assessment.
Adult
500-1000 mL IV initially; then slowly correct fluid deficit over 24-48 h IV
Average daily requirements of sodium and chloride are 1000 mL/d of 0.9% NaCl
Pediatric
Initial bolus: 10-20 mL/kg IV
Maintenance: Slowly correct fluid deficit over 24-48 h IV
May decrease levels of lithium when administered concurrently
Fluid retention; hypernatremia (unless used as a resuscitation fluid)
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
If cerebral edema develops, restrict fluid replacement to two thirds of normal maintenance and replace the deficit over 48 or more h; caution in congestive heart failure, hypertension, edema, liver cirrhosis, renal insufficiency, or sodium toxicity
Insulin
Insulin is the only treatment that addresses the cause of diabetic ketoacidosis. Results from a prospective study of diabetic ketoacidosis suggested the risk of cerebral edema was higher in those who received immediate insulin treatment and starting insulin infusion one h after fluid resuscitation has begun is suggested.
Intravenous insulin is probably the safest and most effective method for treating severe diabetic ketoacidosis. To reduce the risk of hypoglycemia, infuse the insulin through a Y-site or 3-way connector into the same intravenous line used for the maintenance fluid.
Only regular or fast-acting analogue insulins are suitable for intravenous use. Frequent, small subcutaneous doses of insulin lispro or insulin aspart have been used successfully to treat milder cases of diabetic ketoacidosis in which oral fluid replacement is possible. Once the child has recovered, administer subcutaneous insulin for further diabetes maintenance. Administer subcutaneous insulin at least 30 minutes before discontinuing the intravenous insulin.
Insulin regular (Humulin)
A short-acting form of insulin traditionally used in the management of DKA as it may be used intravenously. Stimulates proper use of glucose by the cells and reduces blood sugar levels.
Have pharmacy prepare the syringe at a concentration of 1 U/mL (ie, 50 U insulin qs with 0.9% NaCl to 50 mL). Because of adsorption of insulin to the tubing and syringe, the actual amount of insulin administered may be less than the apparent amount. Adjust doses according to effect and not apparent insulin dose.
Adult
0.05-0.1 U/kg/h IV infusion; adjust dose as needed
Pediatric
Administer as in adults
Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, PO contraceptives, diazoxide, dobutamine phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin
Medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone
Documented hypersensitivity; hypoglycemia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Monitor electrolytes to avoid hypokalemia or hypoglycemia
Insulin lispro (Humalog)
A novel, short-acting, recombinant human insulin analogue that can be given IV to manage DKA. Insulin lispro is an insulin analog that has a more rapid onset and shorter duration of action than regular human insulin.
Stimulates proper use of glucose by the cells and reduces blood sugar levels. Have pharmacy prepare the syringe at a concentration of 1 U/mL (ie, 50 U insulin qs with 0.9% NaCl to 50 mL). Because of adsorption of insulin to the tubing and syringe, the actual amount of insulin administered may be less than the apparent amount. Adjust doses according to effect and not apparent insulin dose.
Adult
0.05-0.1 U/kg/h IV infusion; adjust dose as needed
Pediatric
Administer as in adults
Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, PO contraceptives, diazoxide, dobutamine phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin
Medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone
Documented hypersensitivity; hypoglycemia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Monitor blood glucose and electrolytes to avoid hypoglycemia or hypokalemia
Insulin aspart (NovoLog)
Homologous with regular human insulin with the exception of single substitution of amino acid proline by aspartic acid in position B28. Produced by recombinant DNA technology. Insulin lowers blood glucose levels by stimulating peripheral glucose uptake, especially by skeletal muscle and fat and by inhibiting hepatic glucose production. Inhibits lipolysis in the adipocyte, inhibits proteolysis, and enhances protein synthesis. Insulin is principal hormone required for proper glucose use in normal metabolic processes.
Adult
0.05-0.1 U/kg/h IV infusion; adjust dose as needed
Pediatric
Administer as in adults
Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, PO contraceptives, diazoxide, dobutamine phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin
Medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone
Documented hypersensitivity; hypoglycemia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Monitor blood glucose and electrolytes to avoid hypoglycemia or hypokalemia
Electrolyte replacement
Patients with diabetic ketoacidosis always have a total body deficit of potassium. After initial resuscitation, and provided serum or plasma levels are below 5 mEq/L, or a good renal output has been maintained, add potassium to all replacement fluids.
Potassium chloride
Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function.
Adult
Serum levels >2.5 mEq/L: 10 mEq IV infused over 1 h, and prn based on frequently obtained lab values; not to exceed 200 mEq/24h
Serum levels <2.5 mEq/L: Up to 40 mEq IV infused over 1 h, and prn based on frequently obtained lab values; not to exceed 400 mEq/24h
Pediatric
Serum potassium <2.5 mEq/L: Carefully monitor administration of 1 mEq/kg by separate IV infusions over 1 h
Serum potassium 2.5-3.5 mEq/L: Up to 40 mEq/L in maintenance IV infusion fluid
Serum potassium 3.5-5 mEq/L: 20 mEq/L in maintenance IV infusion fluid
Serum potassium 5-6 mEq/L: 10 mEq/L in maintenance IV infusion fluid
Serum potassium >6 mEq/L: Stop potassium IV infusion and repeat level in 2 h
Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; in patients taking digoxin, hypokalemia may result in digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin
Hyperkalemia, renal failure, and conditions in which potassium retention is present and those with oliguria or azotemia, crush syndrome, severe hemolytic reactions, anuria, and adrenocortical insufficiency
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Do not rapidly infuse; high plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest (must dilute with IV solution prior to administration); plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG; when a concentration >40 mEq/L is infused IV, local pain and phlebitis may also follow
Osmotic diuretics
These agents are used for emergency treatment of cerebral edema. Urgent treatment is required if neurological status deteriorates and hypoglycemia is excluded; delay beyond 10 minutes is associated with very poor outcomes.
Mannitol (Osmitrol, Resectisol)
An osmotic diuretic traditionally used to treat cerebral edema. It is presented as a 10% or 20% solution for infusion, the latter being preferable for pediatric use.
Adult
0.2-0.5 g/kg over 15-20 min (1-2.5 mL/kg of 20% solution); can be repeated after 1 h
Pediatric
Administer as in adults
May decrease serum lithium levels
Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Carefully evaluate cardiovascular status before rapid administration of mannitol because a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination (when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution); do not give electrolyte-free mannitol solutions with blood
Hypertonic saline (3% NaCl)
A hypertonic solution of sodium chloride that can be used as an alternative to mannitol in the treatment of cerebral edema caused by diabetic ketoacidosis.
Adult
250 mL IV bolus
Pediatric
5-10 mL/kg IV administered over 30 min
Alternatively, may be administered as an infusion of 0.1-1 mL/kg/h
None reported
Renal failure; coagulopathies
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in patients with cardiac disease, hypertension, epilepsy, or serious renal impairment
More on Diabetic Ketoacidosis |
| Overview: Diabetic Ketoacidosis |
| Differential Diagnoses & Workup: Diabetic Ketoacidosis |
 Treatment & Medication: Diabetic Ketoacidosis |
| Follow-up: Diabetic Ketoacidosis |
| Multimedia: Diabetic Ketoacidosis |
| References |
| « Previous Page | Next Page » |
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Further Reading
Keywords
diabetic ketoacidosis, DKA, cerebral edema, DKA, diabetes, diabetes mellitus, insulin deficiency, hyperglycemia, low bicarbonate, acidosis, ketonemia, ketonuria, type 1 diabetes, type 1 diabetes mellitus, insulin-dependent diabetes, IDD, insulin-dependent diabetes mellitus, IDDM, childhood diabetes, childhood diabetes mellitus, childhood-onset diabetes, childhood-onset diabetes mellitus, diabetes in childhood, diabetes mellitus in childhood, juvenile-onset diabetes, juvenile-onset diabetes mellitus, ketosis-prone diabetes, autoimmune diabetes mellitus, brittle diabetes mellitus, maturity-onset diabetes of the young, MODY, chamber-pot dropsy, thirst disease, sugar disease, sugar sickness, hypokalemia, hypoglycemia, hyponatremia, acute respiratory distress syndrome, ARDS, pneumothorax, rhabdomyolysis, acute renal failure
