| Diabetic Ketoacidosis | | Counselor, Diabetic ketoacidosis (DKA) is the acute, major, life- threatening complication associated with diabetes mellitus. DKA can occur in either Juvenile or Adult onset diabetes. DKA is defined clinically as an acute state of severe uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids. Biochemically, DKA is defined as an increase in the serum concentration of ketones greater than 5 mEq/L, a blood glucose level of greater than 200 mg/dL, and a blood pH of less than 7.2. The condition can strike even in otherwise healthy well-controlled diabetics and produce dire consequences. We value all your comments, so, if you have a suggestion for a newsletter subject but haven't submitted it yet, or if you have already submitted one but think of another, please take a minute to let us know by clicking on your "Reply" button and dropping us a note. To learn more about AMFS, Inc., the organization run by Physicians and Attorneys that provides medical experts and case review services nationwide, and has produced the following informational newsletter to aid you in understanding complex medical issues, please click here - www.medicalexperts.com. |
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|  Pathophysiology: Technically, DKA usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counter-regulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). This type of hormonal imbalance enhances hepatic gluconeogenesis, glycogenolysis, and lipolysis, the result of which is hyperglycemia, ketone production, and resulting metabolic acidosis. Respiratory compensation of this acidotic condition results in rapid shallow breathing (Kussmaul respirations). Ketones induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA. Increased serum glucose results in increased renal secretion of water as an osmotic diuresis of as much as 6 liters, resulting in dehydration. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. Typical overall electrolyte loss includes 200-500 mEq/L of potassium, 300-700 mEq/L of sodium, and 350-500 mEq/L of chloride. The combined effects of serum hyperosmolarity, dehydration, and acidosis result in increased osmolarity in brain cells that clinically manifests as an alteration in the level of consciousness. |
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| Frequency/Morbidity/Mortality: DKA accounts for 50% of diabetes-related admissions in young persons and 1-2% of all primary diabetes-related admissions. The incidence is estimated to be 1 out of 2000. When DKA is treated properly and expeditiously, it rarely causes any residual effects. However, the overall mortality rate from DKA still ranges from 1-10% of all DKA admissions. Cerebral edema remains the most common cause of mortality, particularly in young children and adolescents. Cerebral edema frequently results from rapid intracellular fluid shifts. Other causes of mortality include severe hypokalemia, adult respiratory distress syndrome, and comorbid states (eg, pneumonia, acute myocardial infarction). |
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| | History/Physical: Insidious increased thirst (ie, polydipsia) and urination (ie, polyuria) is the most common history given by patients with early symptoms of DKA. Nausea and vomiting usually occur and may be associated with diffuse abdominal pain. Generalized weakness and fatigability may occur. Altered consciousness in the form of mild disorientation or confusion is a possible symptom. Symptoms of possible associated intercurrent infection may include fever, dysuria, coughing, malaise, and arthralgia, among others. Patients may present with a history of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons. Physical signs include signs of dehydration - Weak and rapid pulse, dry tongue and skin, hypotension, and increased capillary refill time; a characteristic fruity ketone odor on their breath; rapid shallow breathing which is characteristic of acidosis, abdominal tenderness, and altered levels of consciousness, and signs of concurrent illness including fevers, infections, abscesses, or myocardial infarctions. |
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| | Causes: The following can cause DKA: Insulin deficiency due to poor medication compliance or increased body requirements, concurrent illness such as serious infections or states that lead to dehydration, and the interaction of several medications including corticosteroids. |
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| |  Lab Studies: Urine can easily and quickly be tested. This test is highly positive for glucose and ketones by dipstick testing. The blood glucose level usually is higher than 250 mg/dL, but can be as low as 200 mg/dl. Serum ketones are present. Arterial blood gases (ABG) frequently show typical manifestations of metabolic acidosis, low bicarbonate, and low pH (<7.2). Serum potassium levels initially are high or within the reference range due to the extracellular shift of potassium in exchange of hydrogen, which is accumulated in acidosis, in spite of severely depleted total body potassium. Thus, if a potassium blood level is normal or slightly low, then it can be assumed that the total body potassium is severely depleted. The serum sodium level usually is low. The serum chloride levels and phosphorus levels always are low. The anion gap is elevated ([Na + K] - [Cl + HCO3] >13 mEq/L). Blood tests for glucose should be performed hourly (until patient is stable, then every 6 h). Serum electrolyte determinations should be obtained hourly (until patient is stable, then every 6 h). A CXR should be performed to rule out pneumonia. An MRI of the brain should be performed to rule out cerebral edema if the patient has an altered level of consciousness. An ECG should be performed to rule out a myocardial infarction, or cardiac signs of disturbed potassium levels. |
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| | Treatment: DKA is always managed in an ICU during the first 24-48 hours. When treating DKA, the points that must be considered and closely monitored include correction of fluid loss with IV fluids; correction of hyperglycemia with insulin; correction of electrolyte disturbances, particularly potassium loss; correction of acid-base balance; and treatment of concurrent infection if present. Paying great attention to the correction of fluid and electrolyte loss during the first hour of treatment, followed by gradual correction of hyperglycemia and acidosis, always is advisable. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration means that at least 3 liters of fluid already have been lost. The actual treatment protocol of DKA is beyond the scope of this paper because it is complex. |
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| | Complications: Cerebral edema is a serious, major complication that may evolve during treatment of DKA. Deterioration of the level of consciousness in spite of improved metabolic state usually indicates the occurrence of cerebral edema. MRI usually is used to confirm the diagnosis. If cerebral edema occurs at initiation of therapy, it usually worsens during the course of treatment. Clinical cerebral edema is rare and carries the highest mortality rate. Although mannitol (0.25-1.0 g/kg IV) and dexamethasone (2-4 mg q6-12h) frequently are used in this situation, no specific medication has proven to be useful in such instances. Cardiac dysrhythmias may occur secondary to severe hypokalemia and/or acidosis either initially or as a result of therapy. Usually, correction of the cause is sufficient to treat cardiac dysrhythmia, but, if it persists, consultation with a cardiologist is mandatory. Performing cardiac monitoring on patients with DKA during correction of electrolytes always is necessary. Pulmonary edema may occur for the same reasons as cerebral edema. Although it is rare, one must be cautious of possible overcorrection of fluid loss. Diuretics and oxygen therapy are often sufficient for the management of pulmonary edema. |
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| | Indications for Discharge from the Hospital: Patients are not usually discharged from the hospital unless they have switched back to their daily insulin regimen without recurrence of ketosis. When the condition is stable, pH is greater than 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by an SC dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. |
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| | Medical/Legal Concerns: Adverse outcomes often occur in the following situations: Failure to diagnose DKA in the absence of a urinary test result that is positive for ketones since the urine test may only test for one form of ketone when there are actually others; failure to recognize associated conditions, eg, myocardial infarction, urinary tract infection, pneumonia, perinephric abscess, or hidden sepsis; failure to recognize signs and symptoms of cerebral edema; too rapid correction of hyperglycemia in the first 4-5 hours resulting in electrolyte abnormalities and brain edema; overly rapid correction of metabolic acidosis with sodium bicarbonate before correction of fluid loss resulting in paradoxical CNS acidosis; missing severe hypokalemia by stopping monitoring of serum potassium after it returns to the reference range; and, infusing potassium chloride without continuous monitoring of serum potassium or ECG. All of the aforementioned pitfalls may result in the patient's death, and all of these complications are preventable if DKA is treated properly. |
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