Diabetic Ketoacidosis (DKA), brief description, diagnosis and management simplified

By | March 23, 2017
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Diabetic ketoacidosis (DKA) is a potentially life threatening complication of diabetes mellitis. DKA occurs predominantly  in patients with type 1 diabetes and may be the presenting manifestation. It can also occur in patients with type 2 diabetes under certain circumstances. It results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies that cause most of the signs and symptoms.

 

ETIOLOGY:

DKA results from insulin insufficiency with a relative or absolute increase in glucagon and may be caused by insufficient or interrupted insulin therapy, infections (pneumonia, urinary tract infection, gastroenteritis, sepsis), infarction (cerebral, coronary, mesenteric, peripheral), emotional stress, excessive alcohol intake, surgery, pregnancy and trauma, and certain drugs such as steroids, cocaine etc.

 

CLINICAL PRESENTATION:

DKA clinically presents as polydypsia (excessive intake of fluid due to pronounced thirst), polyuria (excessive urination) anorexia (loss of appetite), nausea or vomiting, abdominal pain, rapid breathing (kussmaul respiration), fruity breath odor of acetone, fever, tachycardia, hypotension, signs of dehydration (dry skin and mucous membranes and poor skin turgor) and altered consciousness to coma.

LABORATARY FINDINGS AND DIAGNOSIS:

DKA is characterised by hyperglycemia, ketosis and metabolic acidosis (increased anion gap) along with a number of secondary metabolic derangement. The serum blood glucose is usually elevated (RBS > 250 mg/dL), ketones in the blood (serum ketones) and on urinalysis are positive, serum bicarbonate is less than 10 mmol/L, and arterial PH ranges between 6.8 to 7.3, depending upon the severity of acidosis.

 

MANAGEMENT:

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  1. Confirm the diagnosis of DKA(elevated blood sugar, positive serum/urinary ketones, metabolic acidosis-low serum bicarbonate and low blood PH).
  2. Admit to hospital; intensive-care setting may be necessary for frequent monitoring or if pH <7.00 or unconscious.
  3. Assess:Serum electrolytes (K+, Na+, Mg2+, Cl–, bicarbonate, phosphate) Acid-base status—pH, HCO3–, PCO2, β-hydroxybutyrate Renal function (serum creatinine, urine output).
  4. Replace fluids:2-3 L of 0.9% saline over first 1-3 hours (10-20 ml/kg per hour). Subsequently, 0.45% saline at 250-500 ml/hour. change to 5% dextrose and 0.45% saline at 150-250 ml/hour when plasma glucose reaches 250 mg/dL. In our setup (KPK, Pakistan) for adults usually 1st L of 0.9% N/S is given in 30 minutes. 2nd liter of 0.9% N/S is given in one hour. 3rd L of 0.9% N/S is given in two hours. 4th L of 0.9% N/S is given in 4 hours and 5th L of 0.9% N/S is given in 8 hours.
  5. administer short-acting insulin: IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by continuous IV infusion; increase 2- to 3-fold if no response by 2–4 h. If initial serum potassium is <3.3 meq/L, do not administer insulin until the potassium is corrected to >3.3 meq/L. If the initial serum potassium is >5.2 meq/L, do not supplement K+ until the potassium is corrected.
  6. Assess the patient: What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, chest x-ray, ECG). The agent or event that precipitated DKA should be aggressively treated. Give IV antibiotics in case of infection. If the patient is vomiting or has altered mental status, a nasogastric tube should be inserted to prevent aspiration of the gastric contents.
  7. Measure capillary glucose every 1-2 hours, measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h.
  8. Monitor blood pressure, pulse, respiration, mental status, fluid intake and output every 1-4 hours.
  9. Replace potassium ions: 10 meq/h when plasma K+ <5.0–5.2 meq/L, ECG normal, urine flow and normal creatinine documented; administer 40–80 meq/h when plasma K+ <3.5 meq/L or if bicarbonate is given.
  10. Continue above until pt is stable,glucose goal is 150–250 mg/dL, and acidosis is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour. when the patient become stable, calculate the dosage of insulin according to the units of short acting insulin given in the last 8 hours.
  11. Administer intermediate or long-acting insulinas soon as pt is eating. Allow for overlap in insulin infusion and SC insulin injection.

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