Diabetic Ketoacidosis
last written: Oct 2011, David LaPierre
last reviewed: Oct 2011, Crystal Sheppy
Introduction
Diabetic ketocacidosis (DKA) is a medical emegency caused by insufficient levels of insulin and increased levels of counter-regulatory hormones such as glucagon, epinephrine, and cortisol. This leads to significant, potentially life-threatening metabolic abnormalities, including hyperglycemia, anion gap metabolic acidosis, hyperketonemia, ketonuria.
The Case of Rachel R
Rachel is a 34 year-old woman with type I diabetes. She has poor control of her sugars during the best of days, and she has not been counting her dietary intake or monitoring her blood glucose over the past two days, as she has been ill with a bad cold. She feels increasingly unwell and comes to the emergency department with nausea, vomiting, and blurred vision.
- What are the symptoms of DKA?
- How is it diagnosed?
- How do you treat someone like Rachel?
Causes and Risk Factors
DKA is more common in Type 1 DM than type II, due to complete insulin deficiency and counter-regulatory hormones.
It is precipitated by the 7 I’s:
- infection (pneumonia, UTI)
- insulin nonadherence/insufficiency (as can occur with pregnancy)
- initial presentation with DMI
- ischemia/infarct (myocardial, stroke, gut)
- inflammation (pancreatitis, cholecystitis)
- iatrogenic (glucocorticoids, dieuretics, surgery)
- intoxication (alcohol, atypical antipsychotics, cocaine)
Pathophysiology
Insufficient insulin levels lead to a change in metabolism. An increase in fatty acid oxidation leads to ketones such as acetone, beta-hydroxybutyrate, and aceto-acetate. This, in turn, leads to an anion gap metabolic acidosis. Acidemia leads to a shift of potassium from cells into the extra-cellular space.
Increased glucose production in liver leads to hyperglycemia and osmotic diuresis, with glycosuria and ketonuria. Dehydration can result, along with electrolyte abnormalities.
Signs and Symptoms
- history
- physical exam
History
Hyperglycemia, dehydration, and electrolyte disturbances can lead to:
- polyuria
- polydipsia
- polyphagia or anorexia
- fatigue
- abdominal pain - can be substantial
- nausea and vomiting
- blured vision
Assess for evidence of infection:
- fever, chills
- GI, respiratory, urinary symptoms
Regarding diabetes management, it is important to inquire into:
- frequency of sugar checks
- diet
- adherence to treatment
- complications, ie diabetic ulcers
- previous admissions for DKA
Ask also about:
- medical conditions
- recent medication changes
- family history
- alcohol, drug use
- social supports
- lifestyle: stress, shiftwork, exercise
- possibility of pregnancy (tigger for DKA)
Physical Exam
Dehydration can lead to:
- postural hypotension
- tachycardia
- JVP
- dry mucous membranes, cracked lips
- reduced skin turgor and tenting
Shortness of breath and Kussmaul respiration (laboured, tachypnic breathing) may be seen in response to metabolic acidosis.
Other signs can include:
- decreased LOC (drowsiness -> stupor -> coma)
- fruity smelling breath (acetone)
- abdominal tenderness, decreased bowel sounds, constipation
- decreased reflexes
Attempt to identify any precipitating infections.
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
Blood
- blood glucose and ketonemia required for diagnosis
- arterial blood gas: anion gap acidosis with possible secondary respiratory alkolosis
- increased BUN and creatinine; may be falsely high due to ketones
- pseudohyponatremia (caused by very high glucose)
- normal or increased K, even though total body K depletion occurs
- low bicarbonate
- phosphorus, calcium, and magnesium may be low
Urine
- ketones
- sugar
- protein
Assessment of causes
- CBC to assess for infection
- tox screen
- amylase and lipase, though can be elevated in DKA independent of pancreatitis
- pregnancy test
Diagnostic Imaging
ECG often shows sinus tachycardia; be sure not to miss acute coronary syndrome, which can precipitate DKA.
Chest X ray should be done to rule out lung infection.
CT head may be considered if a stroke is possible.
Differential Diagnosis
The differential for DKA includes:
- hyperosmolar, nonketotic coma
- alcohol-induced ketoacidosis
- starvation
- overdose, ie ASA
- lactic acidosis
- hypoglycemia
- chronic renal failure
Treatments
Care usually requires hospitalization, often in the intensive care unit for frequent monitoring. Pay attention to mental status, vital signs, and urine output. Assess glucose every hour by finger pick and by blood draw every 2-4 hours, and electrolytes and pH every two hours. Use these parameters to adjust insulin accordingly.
With DKA, treat the anion gap acidosis, rather than the blood sugar. The degree of severity is monitored by anion gap and ketones; with these, there is an increased need for insulin. Most institutions have a protocol - follow these instructions.
ABCs
Monitor especially if patient is in a stupor/coma
- oxygen and airway, as required
- IV access
Rehydration
In a healthy adult, provide 10-20 ml/kg over the first hour, then 500 ml/h for the next few hours, then 250 mg/hr until PO intake resumes. Normal saline is typically used until blood glucose reaches 14 mM/250 mg/dL. At that point, switch to D5/0.45% and maintain sugars between 14-16 mM/150-250 mg/dL.
Caution: aggressive rehydration can lead to congestive heart failure if there is a history of this, or cerebral edema in pediatric patients. Carefully monitor HR, BP, urine output, and JVP.
Insulin therapy
Insulin can be given IV or subcutaneously, with IV recommended in serious cases (ie ketones present). Provide a bolus and then maintenance drip. Again, monitor acidosis and anion gap, as well as glucose. When the anion gap is normal, switch over to subcutaneous insulin, providing an overlap between IV and s.c. A basal insulin can be provided, with a sliding scale of regular insulin adjusted according to specific readings. As values stabilize, shift to the patient's regular home schedule for glucose checks and insulin dosing.
Potassium
DKA depletes the body of potassium, though serum readings may appear high due to cellular shift with acidemia. Hypokalemia is therefore a concern as acidosis is corrected. Monitor the potassium and begin replacing it in the IV as it normalizes. Oral potassium can also be given, but this leads to decreased levels of absorption and may also be compromised by nausea and vomiting.
Be cautious with replacing potassium in renal failure, as the patient may quickly become hyperkalemic.
Other electrolytes
Phosphorus: be cautious replacing, as can lead to hypocalcemia.
Bicarbonate: while bicarbonate was previously used to improve pH, it appears that rehydration usually sufficies.
Magnesium: consider replacement
Pediatrics
If severe vascular decompensation, give a 10 cc/kg bolus with 0.9% NaCl over 30 minutes. Reassess after bolus, repeat if necessary, and otherwise continue. If there is no vascular decompensation, provide:
- <10 kg: 6cc/kg/h
- 10-20 kg: 5 cc/kg/h
- >20 kg: 4 cc/kg/h
Again, be cautious with overhydration, as this can lead to cerebral edema.
Teaching regarding blood sugars - monitoring blood glucose, planning/counting meals, and insulin dosing - should be provided as patients are planning for discharge.
Consequences and Course
DKA a significant cause of diabetes-related deaths. It carries a 2-5% mortality, with marked morbidity from complications. Patients are at increased risk of:
- DVT/PT
- cerebral edema
- respiratory problems
- pulmonary edema and CHF
- hypokalemia (arrhymthias)
- myocardial infarction
- gastritis
- sepsis
- hypoglycemia
Patients are typically well enough to return home if their acidosis is fixed, if they are tolerating oral intake, and if the underlying cause is addressed.
Resources and References
Kitabchi AE et al. 2004. Hyperglycemic crises in diabetes. Diabetes Care. 27:S94-102.
Trachtenbarg DE. 2005. Diabetic Ketoacidosis. Am Fam Physician. 71:1705-14.
Topic Development
authors: Susan Tyler, David LaPierre
reviewers:
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