Diabetic ketoacidosis Flashcards
Define diabetic ketoacidosis.
Biochemical triad of hyperglycaemia, ketonaemia, and acidaemia, with rapid symptom onset due to insulin deficiency.
Most common acute hyperglycaemic complication in type 1 diabetes mellitus
What is the aetiology of DKA?
Reduced circulating insulin and elevation of counter-regulatory hormones: glucagon, catecholamines, cortisol, GH
What are the risk factors for DKA?
- Inadequate/inappropriate insulin therapy
- infection
- MI
- pancreatitis
- stroke
- acromegaly
- hyperthyroidism with concomitant diabetes
- drugs (e.g., corticosteroids, thiazides, pentamidine, sympathomimetics, second-generation antipsychotics, cocaine, immune checkpoint inhibitors, or SGLT-2 inhibitors)
- Cushing’s syndrome with concomitant diabetes
- bariatric surgery
What are the criteria for diagnosis of DKA?
- D: raised blood glucose(>11.1 mmol/L), or known diabetes
- K: ketonuria ++ or more
- A: pH<7.3 (if measured)
- serum bicarbonate <15 mmol/L
Capillary BM should not be relied upon to make a diagnosis
What are the signs and symptoms of DKA?
- polyuria
- polyphagia
- polydipsia
- weight loss
- weakness
- N/V
- abdominal pain
- volume depletion –> dry mucous membranes, poor skin turgor, tachycardia, hypotnesion, sunken eyes
- Kussmaul respiration - rapid and deep due to acidosis
- acenote breath
- reduced GCS
What investigations would you do for DKA?
- Plasma glucose - >13.9mmol/L
- ABG - acidosis (pH 7-7.3) and bicarbonate 10-15
- capillary/serum ketones - beta-hydroxybutyrate elevated ≥3.8 mmol/L or >0.04mg/dL
- urinalysis - glucose, ketones; leukocytes and nitrites in infection
- serum urea - high
- serum creatinine - high
- serum sodium - low
- serum K -usually high
- serum chloride, magnesium, calcium - usually low
- serum phosphate - normal or elevated
- anion gap - increased >10-12 mEq/L
- serum lactate - elevated in lactic acidosis
- FBC - leukocytosis correlated with blood ketone levels
- serum osmolality - varies in DKA; but >320mOsm/kg in HHS
- serum lipase - normal
Which factors would best confirm the diagnosis of diabetic ketoacidosis?
- Metabolic acidosis and a raised capillary blood glucose
- Raised plasma glucose and a metabolic acidosis with an increased anion gap
- Ketonuria and a raised capillary blood glucose
- Acidosis and a history of type 1 diabetes
- Ketonuria and a pH>7.3
Raised plasma glucose and a metabolic acidosis with an increased anion gap
How do you manage DKA?
- IV fluids - correct any shock with 500ml bolus then saline 1-1.5L in the first hour. Check electrolytes hourly. Most are deplete 5-8L.
- Potassium - keep rechecking as demand may increase when you give insulin. If >20mmol/hr given the cardiac monitoring is needed.
- IV insulin once serum potassium >3.3mmol/L - fixed rate 0.1unit/kg/hr
- 10% dextrose - once glucose is <14mmol/L; at rate of 125ml/hr in addition to fluid regimen. Overall 1L over 8hrs.
If they are a previously diagnosed diabetic then continue long acting insulin as normal.
Other:
- vasopressors - dopamine or NA in haemodynamically unstable patients
- bicarbonate therapy - sodium bicarb if pH <7.0
- phosphate therapy - not routinely done unless there is cardiac dysfunction
What are the complications of DKA?
- gastric stasis
- VTE or arterial event - due to inflammation and hyperviscosity
- AKI
Treatment related:
- non-anion gap hyperchloraemic acidosis - due to urinary loss of ketoanions for bicarbonate regeneration
- cerebral oedema/low GCS - avoid over-hydration; younger people <25yrs are most at risk.
- hypoglycaemia - tx related
- hypokalaemia - tx related
- ARDS - tx related reduction in osmotic pressure causing lung pulm oedema
- * underlying sepsis may go undetected *
What is the prognosis with DKA?
mortality is 5% - but death usually relates to an underlying illness
prognosis is worsened at extremes of age and in presence of coma/hypotension
What is the most common PE finding on ECG?
pH 7.06, pO₂ 12.2kPa, pCO₂ 2.2kPa, HCO₃ 8.9mmol/L, BE -11.9. What do these blood gases show?
- Respiratory acidosis
- Type 1 respiratory failure
- Metabolic alkalosis secondary to vomiting
- All values within the normal range
- Metabolic acidosis with partial respiratory compensation
SINUS TACHYCARDIA but S1Q3T3 (deep S1, Q waves in 3 and inverted T waves), AF, right ventricular strain, right axis deviation may also be seen.
E. Metabolic acidosis with partial respiratory compensation
Latest biochemistry and ABG results after 12 hours: Na 135 mmol/L, K 3.9 mmol/L, Ur 7.8 mmol/L, Cr 161 micromol/L, Glu 10.2 mmol/L, pH 7.28 , pO₂ 14.1k Pa, pCO₂ 5.2k Pa, HCO₃ 18.4 mmol/L. Blood ketones:.1.5mmol/L The patient is drinking good volumes of fluids and is anxious to get rid of his drips. What should your next management step be?
- Continue his insulin infusion until blood ketones are <0.6mmol/L
- Continue infusing 0.9% sodium chloride, titrated to his urine output
- Switch to subcutaneous insulin injections
- Stop his intravenous fluids now that he is drinking adequately
- Stop all insulin as his plasma glucose is less than 11.1mmol/L and you risk hypoglycaemia
Continue his insulin infusion until blood ketones are <0.6mmol/L
- He still needs aggressive intravenous fluids until both his acidosis corrects and he clears his ketones, but 10% dextrose can now be used as an additional fluid if his capillary blood glucose is < 14mmols.*
- Subcutaneous insulin may be considered once the patient is eating and has 1+ or less ketones in their urine.*
What electrolyte abnormalities would you get in DKA?
Remember that the anion ‘gap’ estimates unmeasured anions:
(Na+ and K+) – (Cl- and HCO3-) ≈ 10 to 18mmol/L
There is a metabolic acidosis with an increased anion gap in DKA, although this is not exclusive.
Describe a typical fluid regimen in DKA.
When would you give a patient in DKA an intramuscular bolus of 10 units of short acting (soluble) insulin?
If the plasma glucose is greater than 20mmol/L and a delay in starting the insulin infusion is anticipated.
This is followed by an infusion of 50 units of soluble insulin in 50ml 0.9% NaCl using a syringe driver, starting at 0.1 units/kg/hour.
What is the normal plasma osmolality and how is it calculated?
Plasma osmolality is the number of osmoles per kg of solvent.
The normal range is 280-300.
It is elevated in diabetes mellitus.
It can be estimated using the following formula: 2(Na+ + K+) + (urea + glucose)
What are the findings of hyperkalaemia and hypokalaemia on ECG?
Hyperkalaemia can cause
- tall T waves,
- small P waves
- widening of the QRS complex.
Hypokalaemia can lead to
- small or inverted T waves,
- a prolonged PR interval
- ST segment depression.
There is a metabolic acidosis with an increased anion gap in DKA, although this is not exclusive. What else can cause it?
It also occurs in other situations where there is increased production of fixed or organic acids, such as phosphates, ketones and lactate e.g.
- lactic acidosis,
- raised urate in renal failure
- poisoning with salicylates or biguanides
Anion ‘gap’ estimates unmeasured anions:
- (Na+ and K+) – (Cl- and HCO3-) ≈ 10 to 18mmol/L
How is insulin prescribed in DKA?
Actrapid 50units in 50ml 0.9% NaCl at a rate of 0.1units/kg/hr (max 15 units/hr)
Long acting insulin (e.g. Detemir, Glargine, Degludec, Humulin 1) by SC
How do you assess response to treatment in DKA?
Monitoring regimen:
- Hourly BMs
- Hourly capillary ketones
- Venous bicarb and potassium at 60mins, 2hrs then 2hrly
- 4-hourly U&Es
- +/- continuous cardiac monitoring
- +/- continuous pulse oximetry
Expect:
- Ketones falling by 0.5mmol/l/hr
- VBG bicarb rising by 3mmol/l/hr
- Glucose falling by 3mmol/l/hr
When can you discharge someone with DKA?
Ketones <0.6mmol/L
Venous pH >7.3
SC insulin started
eating and drinking
What is the typical potassium regimen in DKA?
When might you consider HDU for DKA?
Young 18-25yrs
Elderly
Pregnant
HF or CKD or other serious co-morbidities
Severe DKA
Venous pH <7.1
What are the severities of DKA?
What are the severities of DKA based on pH?
pH 7.25-7.3 = mild
pH 7.0-7.25 =moderate
pH <7.0 = severe
What is the complication associated with giving bicarbonate in DKA?
Paradoxical acidosis - CO2 will enter CNS when bicarbonate is given peripherally; this causes CNS pH to drop causing a paradoxical acidosis.
