Dibetic ketoacidosis Medical Presentation

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Published on : Jan 12, 2018 | Views : 1890 | Downloads : 3

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MANAGEMENT OF DKA Presented by: Dr. anam mehmood
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Case A 24 year old female with past medical history of diabetes mellitus I is brought to the ER by her mother with complaints of fatigue and increased thirst and urination. Of note patient states she ran out of her insulin last week. She also has had a runny nose and cough for the past week. She noticed her glucose levels have been running “very high” and got concerned. On Exam: BP 101/72; heart rate: 113; respirations: 32; Temperature: 36.8 °C; pulse oximetry: 100% on room air. HEENT: dry mucous membranes CV: tachycardic, normal s1, s2. No murmurs Lung: NVB+0 Abdomen: +bs, non distended, slight tenderness to deep palpation, no rebound or guarding no cyanosis, clubbing or edema
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Case (contin…) LAB RESULTS EKG sinus tachycardia Biochemistry Na: 124, K: 5.0, Cl: 95 BUN: 38, Cr: 1.8 Glucose 450 AST:40, ALT:41, Alk phos:67 Arterial blood gas: pH 6.9, CO2 9, bicarb 10 WBC 13K, Hb14.4 mg/dL, and Hct 43.5%. 75% neutrophils
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UA +glucose, +protein, -leuko esterase, -nitrite NO KETONES Serum ketones test ordered is positive for beta-hydroxybutyrate
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Likely Diagnosis!!!!! Dibetic ketoacidosis
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Dibetic Ketoacidosis DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%.
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Dibetic Ketoacidosis: Definition A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics
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Precipitating Factors: New onset of type 1 DM: 25% Infections (the most common cause): 40% Drugs: e.g. Steroids, Thiazides, Dobutamine & turbutaline. Omission of Insulin: 20%. This is due to: Non-availability (poor countries) fear of hypoglycemia rebellion of authority fear of weight gain stress of chronic disease
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Assessment: History: Symptoms of hyperglycemia, precipitating factors diet and insulin dose. Examination: Look for signs of dehydration, acidosis, and electrolytes imbalance, including shock, hypotension, acidotic breathing, CNS status…etc. Look for signs of hidden infections (Fever strongly suggests infection) and If possible, obtain accurate weight before starting treatment.
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Management: The management steps of DKA includes: Assessment of causes & sequele of DKA by taking a short history & performing a brief examination. Quick diagnosis of DKA at the ER. Baseline investigations. Treatment, Monitoring & avoiding complications. Transition to outpatient management.
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Diagnosis: You should suspect DKA if a diabetic patient presents with: Dehydration. Acidotic (Kussmaul’s) breathing, with a fruity smell (acetone). Abdominal pain &\or distension. Vomiting. An altered mental status ranging from disorientation to coma.
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Diagnosis: To diagnose DKA, the following criteria must be fulfilled : Hyperglycemia: of > 300 mg/dl & glucosuria Ketonemia and ketonuria Metabolic acidosis: pH < 7.25, serum bicarbonate < 15 mmol/l. Anion gap >10. Anion gap= [Na]+[K] – [Cl]+[HCO3]. This is usually accompanied with severe dehydration and electrolyte imbalance.
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Diagnostic Criteria for DKA:
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Diagnostic Studies in DKA Chemistry  Glucose  Bicarbonate Anion gap = (Na+) – (Cl- + HCO3-) Frequently seen:  BUN/creatinine (dehydration)  potassium  sodium Pseudohyponatremia: to correct, add 1.6 mEq of sodium to every 100mg/dL of glucose above normal Serum acetones Positive in DKA
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Diagnostic Studies in DKA (continued..) Urinalysis Ketones (for DKA); leukocyte esterase, WBC (for UTI) CBC Leukocytosis (possible infection) Amylase/Lipase To evaluate for pancreatitis BUT, DKA by itself can also increase them! EKG Evaluate for possible MI
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MANAGEMENT
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MANAGEMENT: Correction of fluid loss with intravenous fluids Correction of hyperglycemia with insulin Correction of electrolyte disturbances, particularly potassium loss Correction of acid-base balance Treatment of concurrent infection, if present
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Correction of Fluid Loss: Determine hydration status: Hypovolemic shock: Administer 0.9% saline, Ringer’s lactate or a plasma expander as a bolus dose of 20-30 ml/kg. This can be repeated if the state of shock persists. Patient needs to be catheterized to measure the urine output to forsee Acute kidney injury.
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Correction of Fluid Loss: B- Dehydration without shock: Initially correction is by isotonic saline, recommended schedule is: Administer 1-3 L during the first hour. Administer 1 L during the second hour. Administer 1 L during the following 2 hours Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings BSL<180mg/dl …. Switch to 5-10% dextrose with half isotonic saline.
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Insulin Therapy: Short acting insulin i.e regular Insulin is the best choice. The initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available, at a rate of 0.1 U/kg/h. A mix of 24 units of regular insulin in 60 mL of isotonic sodium chloride solution usually is infused at a rate of 15 mL/h (6 U/h) until the blood glucose level drops to less than 180 mg/dL; the rate of infusion then decreases to 5-7.5 mL/h (2-3 U/h) until the ketoacidotic state abates. The optimal rate of glucose decline is 100 mg/dL/h. If insulin pump is not available, IV insulin can be givenly hourly i.e Loading dose of 10U followed by 6U/hr, adjusted according to Bsl.
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Electrolyte Correction: Potassium replacement: If K >6mEq/L no replacement If K 4.5-6mEq/L administer 10mEq/L If K 3-4.5mEq/L administer 20mEq/L Usually rule of thumb: 20mEq/L in alternate drip Correction of Acid base balance: IV sodium bicarbonate only in case of decompensated acidosis.
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Metabolic Acidosis:
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Treatment of Concurrent Infection In the presence of infection, the administration of proper antibiotics is guided by the results of culture and sensitivity studies. Starting empiric antibiotics on suspicion of infection until culture results are available may be advisable.
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Monitoring A flow chart must be used to monitor fluid Balance, urine output & Lab measures. serum glucose must be measured hourly. electrolytes also 2-3 hourly. ABGs and urine ketones atleast 4 hourly Ca, Mg, & phosphate must be measured initially & at least once during therapy. Neurological & mental state must examined frequently, & any complaints of headache or deterioration of mental status should prompt rapid evaluation for possible cerebral edema.
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When to shift to S/C Insulin When urinary ketones are negative (Atleast 2 consecutive sets) Anion gap closes Patient becomes conscious and starts tolerating orally Acidosis settles
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Treatment complications: Cerebral edema Rare, but life threatening Usually in pediatric, adolescent patients Symptoms: Headache, altered mental status Treat with mannitol, hyperventilation Myocardial infarction, DVT/PE, cardiac dysrhythmias AKI (acute tubular necrosis, hypovolemia) Hypoglycemia, Hypokalemia Hypophosphatemia Occurs after aggressive hydration/treatment Monitor phosphorus and replete as needed to keep > 1
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PREVENTION of DKA: Type 1 diabetes Education around sick day management Continuation of insulin even when not eating Frequent monitoring when ill Type 2 diabetes Education around sick day management Frequent monitoring when ill
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Thank you
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