Diabetic Ketoacidosis (DKA)

Background/Epidemiology

  • Medical emergency- has a 2% mortality in the UK
  • Complication associated with Type 1 Diabetes– occurs in 1-5% of patients with T1DM (20% in undiagnosed patients)
  • Triad of hyperglycaemia, acidosis and ketosis.

Precipitating Factors (Aetiology)

  • Poor compliance with insulin treatment
  • Bacterial infection and concurrent illness (not uncommonly, Klebsiella pneumonia)
  • Medical, surgical or emotional stress
    • e.g. hypothyroidism, cardiovascular disease, stroke, MI
    • e.g. pregnancy, trauma
    • drugs e.g. steroids, sympathomimetics, α- and β-blockers

Pathophysiology

  • The main biochemical features are
    • Hyperketonaemia (≥3mmol/l) and ketonuria (more than 2+ on dipstick)
    • Hyperglycaemia (blood glucose ≥11mmol/l)
    • Metabolic Acidosis (venous bicarbonate <15mmol/l and/or venous pH <7.3)
  • Hyperglycaemia causes osmotic diuresis, leading to dehydration and electrolyte loss (particularly sodium and potassium)
    • Potassium loss is exacerbated by secondary hyperaldosteronism due to decreased kidney perfusion, as well as the acidosis caused by ketones, which drives H+ into the cells and K+ out
      • NB (Almost) ALL patients with DKA will be low in potassium but blood levels can be false normal due to K+ displacement by H+ and due to concomitant water loss**
  • Ketosis results from insulin deficiency, exacerbated by increased catecholamines and other stress hormones, leading to massive lipolysis and supply of FFAs for ketogenesis.
    • If and when this exceeds the capacity of the liver to metabolise the ketones, they begin to accumulate in the blood, resulting in acidosis
  • Water and electrolyte loss can be severe in DKA (intracellular loss initially asymptomatic -> extracellular loss becomes symptomatic later)

Presentation

  • It is often useful to ask about common precipitants (e.g. fever, dyspnoea, chest pain, palpitations, abdominal pain, change in medication, alcohol consumption, change in diet etc)
  • Symptoms are almost that of a severe presentation of T1DM i.e.
    • Polyuria, polydipsia (thirst), weight loss
    • Other features include weakness, nausea and vomiting (vague abdominal pain is also very common in young children), myalgia, visual disturbance (blurry vision)
  • Signs
    • Common signs can be tachycardia, breathlessness, confusion
    • Signs of dehydration can be difficult to see (often more apparent in severe cases)
      • e.g. dry mucous membranes, loss of skin turgor, furred tongue, cracked lips, sunken eyes, hypotension
    • A unique sign for DKA is the sweet-smelling/fetid smelling breath
    • Reduced consciousness and coma is relatively uncommon but can occur

Investigations

  • NB If DKA is clinically suspected, do not delay treatment for investigations/results.
  • Blood tests
    • FBC- WBC may be raised but does not (always) indicate infection; CRP
    • U&Es- Hypernatraemia (dehydration) or hyponatraemia (glucose/ketone interference); Hyperkalaemia is common (due to acidosis but patients will be deplete of K intracellularly); urea/creatinine may be high if renal function is impaired
    • ABGs– metabolic acidosis (low pH, low HCO3; usually normal pCO2 but can be low due to respiratory compensation; pO2 also usually normal unless underlying respiratory problem)
    • If available, ketone measurements
    • Glucose
  • BM blood glucose
  • Urinalysis (glycosuria and ketonuria) and microscopy and culture
  • CXR and ECG are also routinely performed in the acute setting

Diagnosis

  • Capillary (BM) Blood Glucose >11mmol/l
  • Capillary ketones >3mmol/l or Urinary ketones ++ or more
  • Venous pH <7.3 and/or Bicarbonate <15mmol/l

Management

  • EMERGENCY- treat in hospital/HDU.  NB If diagnosis unknown/acute setting, manage with ABCDE
  1. Immediate Management (0-60 mins)
    1. Commence IV 0.9% saline
      1. If SBP<90mmHg
        1. Give 500ml over 10-15 mins.  If SBP remains <90mmHg, repeat and seek senior advice.
        2. Consider involving ITU/Critical care (depending on patient symptoms e.g. change in consciousness)
        3. If SBP increases to >90mmHg, give 1000ml 0.9% saline over next 60 mins.
          1. NB Patient can become rapidly hypokalaemic with fluid replacement and may require supplementation
            • If >5.5mmol/l – none; if 3.5-5.5mmol/l – give 40mmol/l; if <3.5mmol/l – get senior review, more potassium required
    2. Commence IV insulin infusion (0.1 unit/kg/hour; 50 units in 50ml of 0.9% saline)
      1. NB If the patient is also on a long-acting insulin, continue this as normal
    3. Assess patient
      1. Resp rate, temperature, BP, Pulse, saturation
      2. GCS
      3. Full head-toe examination
      4. Investigations e.g. capillary and laboratory glucose, Venous/Arterial BGs; U&Es, FBC; Blood cultures; ECG; CXR; MSSU
    4. Monitor
      1. Hourly BM and capillary blood ketones; measure venous bicarbonate and potassium at 60 and 120 minutes then every 2 hours
      2. Measure electrolytes every 4 hours
      3. Consider any other causes and manage appropriately
    5. NB A central line may be appropriate in young/old people, pregnant women, Heart/kidney problems, serious comorbidity, severe DKA 
      1. e.g. Ketones >6 mmol/l; Venous bicarb <5mmol/l; venous pH <7.1; hypokalaemia on admission, GCS<12, O2 sats <90%; BP<90mmHg, pulse >100 or <60
      2. Anion gap
  2. Management at 1-6 hours (Resolution/Maintenance)
    1. Monitor the patients (hourly blood glucose and ketones, venous BGs and potassium if it’s abnormal
    2. Continue fluid replacement
      1. 1l 0.9% saline with KCl over 2 hours (×2)
      2. 1l 0.9% saline with KCl over 4 hours
        1. Add 10% glucose 125ml/hour if blood glucose falls <14mmol/l
    3. Aim
      1. Capillary ketones not dropping by >0.5mmol/l/hour
      2. Venous bicarbonate not rising by >3mmol/l/hour
      3. Plasma glucose not fallinf by >3mmol/l
      4. Continuous IVII until ketones <0.3mmol/l, venous pH >7.3 and/or venous bicarb >18mmol/l
  3. Management at 6-12 hours (if the patient is not improved)
    1. Continue IV fluids at a reduced rate
      1. 1l 0.9% saline with KCl over 4 hours then repeat over 6 hours
        1. Add 10% glucose 125/ml/hour if glucose is <14mmol/l
    2. Re-assess biochemistry at 6 hours e.g. Venous pH, bicarb, potassium, ketones, glucose. Assess CVS risk at 12 hours and check for fluid overload.
      1. Resolution: Ketones <0.3mmol/l ; venous pH >7.3 (bicarb not used)
      2. If not resolved, review IVII and fluids
  4. Recovery
    1. Make sure the patient is eating and drinking
    2. Treat any precipitating factors e.g. infection
    3. Re-assess for complications e.g. fluid overload
    4. Switch to subcut insulin if the patient is recovering ok.
      1. (If not, specialist input is required).
      2. NB Do not stop IVII until 30 mins after first subcut short acting insulin injection

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