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DIABETIC KETOACIDOSIS

It is a major medical emergency & remains a serious cause of morbidity , principally in people with type 1 diabetes. Any form of stress particularly infection can precipitate severe ketoacidosis even in patients with type 2 diabetes.

Pathogenesis

• Diabetic ketacidosis is characterised by

  • Hyperglycemia

  • Hyperketonemia

  • Metabolic acidosis

• Hyperglycemia causes profound osmotic diuresis leading to dehydration & electrolyte loss particularly sodium & potassium.

• Potassium loss is exacerbated by secondary hyperaldosteronism as a result of reduced renal perfusion.

• Ketosis results from insulin deficiency , exacerbated by catecholamines & other stress hormones, resulting in unrestrained lipolysis & supply of free fatty acids for hepatic ketogenesis. When this exceeds the capacity to metabolise they accumulate in blood & produce metabolic acidosis.

FLUID LOSS

CLINICAL FEATURE

Diagnostic criteria

• Blood glucose >250mg/dl

• Arterial pH<7.3

• Bicarbonate <15mEq/L

• Moderate ketonuria or ketoniemia

Investigations

• Hrly GRBS

• Check electrolytes BUN, creatinine every 2-4 hrly

• ABG

• CBC

• URE

• Blood & urine cultures

• ECG, Chest xray

Management

• FLUID REPLACEMENT

  • Normal saline (0.9%) is used to replace the extracellular lose initially

    • 1L/h over the first 1-2 hrs.

    • After the first 2L of fluid has been given, the intravenous infusion should be at the rate of 300 – 400ml/h

  • When blood glucose <15 mmol/L (<270mg/dl)

    • Switch to 5% dextrose 1L 8^th hrly

    • If still dehydrated continue 0.9% saline & add 5% dextrose 1L per 12hrs

• Typical requirement is 6L in first 24 hrs

• Avoid fluid overload in elderly.

• INSULIN

  • Initial bolus dose of 0.1 U/kg is given to prime the insulin receptors followed by 0.1U/kg/h.

  • Recent studies has shown that bolus dose is not required.

  • Insulin dose is adjusted to obtain a fall of 50-70mg/dl/hrly.

• Potassium

• 10 – 30mEq/h should be infused during second & third hrs after beginning therapy as soon as acidosis starts to resolve (if patient has no renal failure).

• If K+ <3.5mEq/L first potassium level is corrected before starting insulin.

• Sodium bicarbonate

  • Bicarbonate therapy is not indicated routinely, unless the pH <7.0 or less , with careful monitoring to prevent overcorrection.

  • Bicarbonate therapy is stopped once pH reaches 7.1 or greater as it may cause rebound metabolic alkalosis as ketones are metabolised. Alkalosis shifts potassium from serum into cells which could precipitate a fatal cardiac arrythmia.

• Antibiotics : Are used as indicated.

• Switching to SC insulin

• SC regimen is started once the patient is awake and able to eat, SC insulin therapy can be initiated.

• Total daily insulin dose of 0.6U/kg is given.

• Total daily dose is calculated from the insulin requirement during the last 8hrs . Half the dose is given as long acting basal insulin & other half as a short acting insulin premeals.

• SC insulin should be given 1hr before stopping the infusion.

COMPLICATION

• Cerebral oedema : It is characterized by sudden onset of headache or deterioration in mental status during treatment . Risk factors for its development include severe baseline acidosis, rapid correction of hyperglycemia and excess volume administration in first 4hrs. IV mannitol 1-2gm/kg is the mainstay of treatment.

• Acute respiratory distress syndrome

• Thromboembolism

• DIC

• Acute circulatory failure

Updated on 27/3/13.

Reference :

• CMDT 2013

• Davidson 21^st edition.