Diabetic Ketoacidosis - Clinicals, Diagnosis, and Management

Emergency Medicine

Clinicals - History

Fact Explanation
Polydipsia Elevated serum glucose increases the serum osmolality. Increased osmolality stimulates the thirst receptors, and hence excessive thirst develops. This is exacerbated by polyuria. Polydipsia
Elevated serum glucose increases the serum osmolality. Increased osmolality stimulates the thirst receptors, and hence excessive thirst develops. This is exacerbated by polyuria.
Polyuria Hyperglycemia causes osmotic diuresis and results in polyuria. Polyuria
Hyperglycemia causes osmotic diuresis and results in polyuria.
Polyphagia This is also a common presentation. Polyphagia
This is also a common presentation.
Abdominal pain Common in children. Abdominal pain is secondary to acidosis and may spontaneously diminish with the correction of metabolic disturbances. Abdominal pain
Common in children. Abdominal pain is secondary to acidosis and may spontaneously diminish with the correction of metabolic disturbances.
Weakness Hyperkalemia results in generalized muscle weakness. Weakness
Hyperkalemia results in generalized muscle weakness.
Nausea and or vomiting This is a common presentation. Vomitus can be Coffee-ground color due to hemorrhagic gastritis. Nausea and or vomiting
This is a common presentation. Vomitus can be Coffee-ground color due to hemorrhagic gastritis.
Symptoms of dehydration Dehydration is common due to polyuria and vomiting. Patients complain of excessive thirst. Symptoms of dehydration
Dehydration is common due to polyuria and vomiting. Patients complain of excessive thirst.
Symptoms of cerebral edema Cerebral edema is a complication of DKA which is commoner in young children than in adults. Headache, confusion, seizures and lethargy are common presentations. Symptoms of cerebral edema
Cerebral edema is a complication of DKA which is commoner in young children than in adults. Headache, confusion, seizures and lethargy are common presentations.
Presence of precipitating factors Infection is a recognized precipitating cause for DKA. Urinary tract infections present with dysuria, increased frequency of micturition and suprapubic pain. Fever, cough, dyspnea and chest pain are suggestive of a respiratory tract infection. Psychological stress, myocardial infarction, congestive cardiac failure, pancreatitis, pulmonary embolism, trauma, poor compliance to insulin therapy and or use of sub therapeutic doses are known precipitating factors. Presence of precipitating factors
Infection is a recognized precipitating cause for DKA. Urinary tract infections present with dysuria, increased frequency of micturition and suprapubic pain. Fever, cough, dyspnea and chest pain are suggestive of a respiratory tract infection. Psychological stress, myocardial infarction, congestive cardiac failure, pancreatitis, pulmonary embolism, trauma, poor compliance to insulin therapy and or use of sub therapeutic doses are known precipitating factors.

Clinicals - Examination

Fact Explanation
Body temperature Body temperature can be either normal or low, even in the presence of infection. But if the patient is febrile infection should be present. Body temperature
Body temperature can be either normal or low, even in the presence of infection. But if the patient is febrile infection should be present.
Kussmaul’s respirations Rapid shallow breathing occurs to compensate for metabolic acidosis. Sometimes the breath has characteristic fruity odor. Kussmaul’s respiration can be absent if the patient develops cerebral edema. Respiratory arrest is seen. Kussmaul’s respirations
Rapid shallow breathing occurs to compensate for metabolic acidosis. Sometimes the breath has characteristic fruity odor. Kussmaul’s respiration can be absent if the patient develops cerebral edema. Respiratory arrest is seen.
Signs of dehydration Patients have reduced skin turgor, sunken eyes, dry mucous membranes and depressed consciousness due to dehydration. Tachycardia and hypotension can also be detected. Signs of dehydration
Patients have reduced skin turgor, sunken eyes, dry mucous membranes and depressed consciousness due to dehydration. Tachycardia and hypotension can also be detected.
Signs of cerebral edema Cerabral edema results in papilledema, hypertension, bradycardia, hyperpyrexia, and altered consciousness. Consciousness is intact in mild DKA but impaired in moderate DKA. Patients can be comatose in severe DKA. Signs of cerebral edema
Cerabral edema results in papilledema, hypertension, bradycardia, hyperpyrexia, and altered consciousness. Consciousness is intact in mild DKA but impaired in moderate DKA. Patients can be comatose in severe DKA.

Investigations - Diagnosis

Fact Explanation
Random blood sugar Hyperglycemia is an essential feature to diagnose DKA. Random blood sugar should be more than 250 mmol /L for the diagnosis of DKA is to be made. Random blood sugar
Hyperglycemia is an essential feature to diagnose DKA. Random blood sugar should be more than 250 mmol /L for the diagnosis of DKA is to be made.
Serum ketone bodies Absolute or relative deficiency of insulin leads to increase in counter regulatory hormones like, glucagon, cortisol, growth hormone, and epinephrine. These catabolic hormones stimulate hepatic gluconeogenesis, glycogenolysis, and lipolysis, resulting in hyperglycemia increased serum free fatty acids. Excess fatty acids are metabolized to ketones and keto acids in the liver, resulting ketosis. Serum ketone bodies
Absolute or relative deficiency of insulin leads to increase in counter regulatory hormones like, glucagon, cortisol, growth hormone, and epinephrine. These catabolic hormones stimulate hepatic gluconeogenesis, glycogenolysis, and lipolysis, resulting in hyperglycemia increased serum free fatty acids. Excess fatty acids are metabolized to ketones and keto acids in the liver, resulting ketosis.
Urinary ketone bodies Excess of ketone bodies in serum leads to ketonuria. This is an essential feature in diagnosis. Urinary ketone bodies
Excess of ketone bodies in serum leads to ketonuria. This is an essential feature in diagnosis.
Arterial blood gas analysis Dehydration and ketosis causes acidosis, which is a constant feature. In mild DKA arterial PH is 7.25 to 7.30. PH of 7.00 to 7.24 is moderate DKA and less than 7.00 is severe DKA. Serum bicarbonate levels are reduced. 15 to 18 mEq/L in mild DKA, 10 to 15 mEq/L in moderate DKA and less than 10 mEq/L in severe DKA. (bicarbonate levels can be normal due to vomiting, diuretic use, or alkali ingestion.) Anion gap is more than 10 in mild DKA, more than 12 in moderate and severe DKA. Arterial blood gas analysis
Dehydration and ketosis causes acidosis, which is a constant feature. In mild DKA arterial PH is 7.25 to 7.30. PH of 7.00 to 7.24 is moderate DKA and less than 7.00 is severe DKA. Serum bicarbonate levels are reduced. 15 to 18 mEq/L in mild DKA, 10 to 15 mEq/L in moderate DKA and less than 10 mEq/L in severe DKA. (bicarbonate levels can be normal due to vomiting, diuretic use, or alkali ingestion.) Anion gap is more than 10 in mild DKA, more than 12 in moderate and severe DKA.
Beta-hydroxybutyrate This is one of the ketone bodies found in serum and accounts for about 75% of the total. Beta-hydroxybutyrate is more than 3 mg per dL in DKA. Beta-hydroxybutyrate
This is one of the ketone bodies found in serum and accounts for about 75% of the total. Beta-hydroxybutyrate is more than 3 mg per dL in DKA.
Serum osmolality In DKA serum osmolality is definitely more than 320 mOsm per kg. if serum osmolality is lower than that alternative diagnoses should be considered. Serum osmolality
In DKA serum osmolality is definitely more than 320 mOsm per kg. if serum osmolality is lower than that alternative diagnoses should be considered.
Glycosylated hemoglobin levels (HbA1C) HbA1C levels will reflect the overall blood sugar control during the past 3 months. Normal HbA1C levels are suggestive of an acute event. Glycosylated hemoglobin levels (HbA1C)
HbA1C levels will reflect the overall blood sugar control during the past 3 months. Normal HbA1C levels are suggestive of an acute event.
Full blood count Aids in diagnosing infections. Full blood count
Aids in diagnosing infections.
Electrocardiography Myocardial infarction is relatively rare but a possible cause of DKA. ECG will aid in making the diagnosis. Electrocardiography
Myocardial infarction is relatively rare but a possible cause of DKA. ECG will aid in making the diagnosis.
Urine full report Diagnose urinary tract infection as the causative factor of DKA. Urine full report
Diagnose urinary tract infection as the causative factor of DKA.
Chest X-ray Aids in diagnosing respiratory tract infection and congestive cardiac failure (chest X-ray will show cardiomegaly, Kerley B lines, pulmonary edema, upper lobe diversion and pleural effusions). Chest X-ray
Aids in diagnosing respiratory tract infection and congestive cardiac failure (chest X-ray will show cardiomegaly, Kerley B lines, pulmonary edema, upper lobe diversion and pleural effusions).
Cultures Blood, urine, respiratory secretions can be cultured to diagnose infection and to isolate the causative organism. Cultures
Blood, urine, respiratory secretions can be cultured to diagnose infection and to isolate the causative organism.

Investigations - Management

Fact Explanation
Random blood glucose Blood glucose levels should be monitored every one or two hourly to monitor the treatment and to adjust the dose of insulin. Random blood glucose
Blood glucose levels should be monitored every one or two hourly to monitor the treatment and to adjust the dose of insulin.
Serum electrolytes Should be repeated every two to six hourly. During the early DKA glomerular filtration rate is decreased and this results in hyperkalemia. Once osmotic diuresis and oliguria develops serum potassium levels tend to decline. With insulin, and bicarbonate treatment potassium levels decrease. Serum electrolytes
Should be repeated every two to six hourly. During the early DKA glomerular filtration rate is decreased and this results in hyperkalemia. Once osmotic diuresis and oliguria develops serum potassium levels tend to decline. With insulin, and bicarbonate treatment potassium levels decrease.
Serum creatinine Serum creatinine is elevated and levels should be repeated every two to six hourly. Serum creatinine
Serum creatinine is elevated and levels should be repeated every two to six hourly.
Blood urea nitrogen Usually elevated. Should be repeated every two to six hourly. Blood urea nitrogen
Usually elevated. Should be repeated every two to six hourly.
Serum bicarbonate Should be repeated every two to six hourly. Serum bicarbonate
Should be repeated every two to six hourly.
Beta-hydroxybutyrate This is used for the monitoring of the treatment. Usually it falls to less than 1.5 mg per dL within the first 12 to 24 hours of treatment. Beta-hydroxybutyrate
This is used for the monitoring of the treatment. Usually it falls to less than 1.5 mg per dL within the first 12 to 24 hours of treatment.
Arterial blood gas analysis This should be repeated to monitor treatment. Arterial blood gas analysis
This should be repeated to monitor treatment.
Serum phosphate Hypophosphataemia can occur with DKA. Serum phosphate
Hypophosphataemia can occur with DKA.
Cardiac monitoring Necessary for patients with electrolyte abnormalities for the early detection of cardiac arrhythmias. Cardiac monitoring
Necessary for patients with electrolyte abnormalities for the early detection of cardiac arrhythmias.
Cerebral imaging CT or MRI scan of the head will help in diagnosing cerebral edema. Dilated ventricles can be seen in CT or MRI. Cerebral imaging
CT or MRI scan of the head will help in diagnosing cerebral edema. Dilated ventricles can be seen in CT or MRI.
Hepatic transaminases Usually elevated but the exact cause is not known. Hepatic transaminases
Usually elevated but the exact cause is not known.

Management - Supportive

Fact Explanation
Treatment setting Patients who are conscious and alert with mild DKA can be treated as outpatients and if arterial pH is below 7.30, and serum bicarbonate level is less than 15 mEq per L patient should be admitted. Patients with severe DKA should be provided intensive care. Treatment setting
Patients who are conscious and alert with mild DKA can be treated as outpatients and if arterial pH is below 7.30, and serum bicarbonate level is less than 15 mEq per L patient should be admitted. Patients with severe DKA should be provided intensive care.
Health education Patients should be educated about the chronic nature of the disease and necessity of life long treatment and follow up. Enough information should be provided on use of insulin, importance of compliance, dietary practices, sick day rules and need of regular blood sugar monitoring. Patients should be aware of early detection of signs of DKA to seek health care early.
Once they are sick and cannot take orally they should seek professional advice to adjust the insulin therapy. Carbohydrates containing fluids can be used to maintain blood sugar levels when the oral intake is reduced.
Health education
Patients should be educated about the chronic nature of the disease and necessity of life long treatment and follow up. Enough information should be provided on use of insulin, importance of compliance, dietary practices, sick day rules and need of regular blood sugar monitoring. Patients should be aware of early detection of signs of DKA to seek health care early.
Once they are sick and cannot take orally they should seek professional advice to adjust the insulin therapy. Carbohydrates containing fluids can be used to maintain blood sugar levels when the oral intake is reduced.
Management of airway and breathing In unconscious patients patency of the airway should be maintained with an oral, nasopharyngeal airway or with an endotracheal tube. A naso-gastric tube may be needed to protect the airway if patient develops vomiting. Breathing is supported with oxygen. Management of airway and breathing
In unconscious patients patency of the airway should be maintained with an oral, nasopharyngeal airway or with an endotracheal tube. A naso-gastric tube may be needed to protect the airway if patient develops vomiting. Breathing is supported with oxygen.
Fluid resuscitation If the patient is in shock 20 ml kg−1 fluid bolus should be administrated. If shock does not improve with that inotropes may be required. Thereafter 15–20 ml · kg−1 body wt · h−1 fluid deficit should be replaced with 0.9% normal saline. Once fluid deficit is replaced and blood pressure is normalized 0.45% saline (4–14 ml · kg−1 · h−1) should be used instead, if the serum sodium is normal or elevated. If serum sodium is low, 0.9% normal saline should be continued. Urine output should be monitored to evaluate the adequacy of fluid replacement. Urine output should reduce with adequate rehydration, as the effect of osmotic diuresis diminishes with reduced blood glucose concentration. Once the blood glucose concentration reaches 250 mg per dL 5% dextrose should be added to 0.45% normal saline to prevent ketosis. Fluid resuscitation
If the patient is in shock 20 ml kg−1 fluid bolus should be administrated. If shock does not improve with that inotropes may be required. Thereafter 15–20 ml · kg−1 body wt · h−1 fluid deficit should be replaced with 0.9% normal saline. Once fluid deficit is replaced and blood pressure is normalized 0.45% saline (4–14 ml · kg−1 · h−1) should be used instead, if the serum sodium is normal or elevated. If serum sodium is low, 0.9% normal saline should be continued. Urine output should be monitored to evaluate the adequacy of fluid replacement. Urine output should reduce with adequate rehydration, as the effect of osmotic diuresis diminishes with reduced blood glucose concentration. Once the blood glucose concentration reaches 250 mg per dL 5% dextrose should be added to 0.45% normal saline to prevent ketosis.
Temperature management Hypothermia should be prevented by using blankets, overhead heating lamps, and warmed intravenous fluids. Temperature management
Hypothermia should be prevented by using blankets, overhead heating lamps, and warmed intravenous fluids.
Potassium replacement Potassium levels are usually high at the time of diagnosis. When insulin is administered serum potassium is taken in to the cells and this can cause hypokalemia. In order to prevent this potassium should be replaced if serum potassium is low or normal. If potassium level is less than 5.5 mEq/L, 20 mEq potassium chloride should be added and if the K+ level is less than 3.3 mEq/L, 40 mEq potassium chloride should be added to the intravenous fluid used. Potassium supplementation should be continued till the patient is fit enough to take orally. Potassium replacement
Potassium levels are usually high at the time of diagnosis. When insulin is administered serum potassium is taken in to the cells and this can cause hypokalemia. In order to prevent this potassium should be replaced if serum potassium is low or normal. If potassium level is less than 5.5 mEq/L, 20 mEq potassium chloride should be added and if the K+ level is less than 3.3 mEq/L, 40 mEq potassium chloride should be added to the intravenous fluid used. Potassium supplementation should be continued till the patient is fit enough to take orally.
Bicarbonate infusion Severe acidosis (PH less than 6.9) should be treated with intravenous bicarbonate, because it shifts the oxygen hemoglobin dissociation curve to the right and reduces tissue oxygenation. In severe acidosis 100 mmol of sodium bicarbonate is added to 400 mL of distilled water and infused over two hours. If PH is between 6.9 to 7.0 doses of NaHCO3 distilled water should be halved (50mmol of sodium bicarbonate and 200ml of distilled water) and infused over two hours. Bicarbonate infusion is stopped once the PH reaches 7.0. Bicarbonate infusion
Severe acidosis (PH less than 6.9) should be treated with intravenous bicarbonate, because it shifts the oxygen hemoglobin dissociation curve to the right and reduces tissue oxygenation. In severe acidosis 100 mmol of sodium bicarbonate is added to 400 mL of distilled water and infused over two hours. If PH is between 6.9 to 7.0 doses of NaHCO3 distilled water should be halved (50mmol of sodium bicarbonate and 200ml of distilled water) and infused over two hours. Bicarbonate infusion is stopped once the PH reaches 7.0.
Treatment of cerebral edema Mannitol (0.5 g kg−1) or hypertonic saline (3–5 ml kg−1 over 10 min) will reduce the cerebral edema. Treatment of cerebral edema
Mannitol (0.5 g kg−1) or hypertonic saline (3–5 ml kg−1 over 10 min) will reduce the cerebral edema.
Treat the precipitant cause Infections should be treated and myocardial infarction and other precipitant causes should be managed accordingly. Treat the precipitant cause
Infections should be treated and myocardial infarction and other precipitant causes should be managed accordingly.
Vaccination Influenza vaccine should be administered annually to prevent respiratory infections which is a common precipitating cause. Vaccination
Influenza vaccine should be administered annually to prevent respiratory infections which is a common precipitating cause.

Management - Specific

Fact Explanation
Insulin This is the definitive form of treatment. 5 to 7 U per hour (0.1 units/kg if the body weight is less than 60kg) should be administered for adults. This rate should be reduced by half once blood sugar levels reach 250 mg per dL. If blood sugar level does not fall by at least 50 to 100 mg/dL hourly dose of insulin should be doubled. Subcutaneous insulin should be used when the blood sugar is around 150 to 200 mg per dL. Insulin
This is the definitive form of treatment. 5 to 7 U per hour (0.1 units/kg if the body weight is less than 60kg) should be administered for adults. This rate should be reduced by half once blood sugar levels reach 250 mg per dL. If blood sugar level does not fall by at least 50 to 100 mg/dL hourly dose of insulin should be doubled. Subcutaneous insulin should be used when the blood sugar is around 150 to 200 mg per dL.

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