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Year 3 > Diabetic ketoacidosis (E&M) > Flashcards

Diabetic ketoacidosis (E&M) Flashcards

1
Q

Define DKA.

A

Acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment

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2
Q

Who does DKA occur in and why?

A

T1DM patients –> no insulin to suppress lipolysis –> ketone formation –> acidosis

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3
Q

What may DKA indicate?

A

Initial presentation in someone with undiagnosed T1DM

(DKA is the most common acute hyperglycaemic complication of T1DM)

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4
Q

Why does ketogenesis occur in DKA?

A

Excessive glucose but insufficient insulin to push it into cells –> body goes into a starvation-like state where ketogenesis is the only mechanism of energy production

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5
Q

What are some precipitating/contributing factors to DKA?

A
  • most common: infection + discontinuation of/inadequate insulin therapy
  • underlying medical conditions e.g. MI or pancreatitis
  • drugs affecting carbohydrate metabolism e.g. corticosteroids, thiazides, sympathetic agents
  • SGLT-2 inhibitors
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6
Q

What are the sick day rules for T1DM patients? (4)

A
  • continue normal insulin dose
  • check BGC more regularly
  • drink 3L of fluid over 24h
  • self-monitor ketones regularly throughout day
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7
Q

What is DKA a biochemical triad of?

A
  1. hyperglycaemia
  2. ketonemia
  3. metabolic acidosis

(With rapid symptom onset)

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8
Q

What are the clinical features of DKA? (9)

A
  • diabetic features (polydipsia, polyuria, weight loss, tiredness)
  • nausea & vomiting
  • abdominal pain
  • dehydration (dry mucous membranes, decreased skin turgor, slow CRT, tachycardic, hypotensive)
  • hyperventilation (Kussmaul breathing)
  • reduced consciousness
  • hypothermia
  • ketotic breath (acetone smell/fruity)
  • rapid onset (<24 hours)
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9
Q

What might you see on examination in DKA? (5 - overlap with clinical features)

A
  • dehydration (dry mucous membranes, decreased skin turgor, slow CRT, tachycardic, hypotensive)
  • hyperventilation (Kussmaul breathing)
  • reduced consciousness
  • hypothermia
  • ketotic breath (acetone smell/fruity)
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10
Q

What are the signs of dehydration in DKA? (5)

A
  • dry mucous membranes
  • reduces skin turgor
  • slow capillary refill time
  • tachycardia (with weak pulse)
  • hypotension
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11
Q

Why does Kussmaul breathing occur in DKA?

A

Decrease in pH stimulates respiratory centre to try and correct acidosis by blowing off CO2 –> deep, rapid, laboured breathing

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12
Q

What are some risk factors for DKA? (6)

A
  • infection (most common precipitating factor)
  • inadequate insulin therapy
  • undiagnosed T1DM
  • MI (or pancreatitis)
  • drugs affecting carbohydrate metabolism e.g. corticosteroids, thiazides, sympathetic agents
  • SGLT-2 inhibitors
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13
Q

Why is infection the most common precipitating factor for DKA?

A
  • increased cortisol in infection (antagonist of insulin) –> body’s insulin requirements increase
  • T1DM patients should make sure they continue taking insulin when unwell to prevent DKA
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14
Q

What are the first-line investigations for DKA? (5)

A
  • venous blood gas (VBG)
  • blood ketones (high)
  • blood glucose (high)
  • U&Es
  • FBC (raised WCC without infection)
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15
Q

What does VBG show in DKA? (4)

A
  • metabolic acidosis with raised anion gap (>16 indicates severe DKA) with partial respiratory compensation (hyperventilation)
  • pH <7.0 indicates severe DKA
  • hyperkalaemia is common (replace K+ if <5.5)
  • high plasma osmolality (>320mmol/kg)
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16
Q

What do U&Es show in DKA? (3)

A
  • hyponatraemia and hyperkalaemia are common due to lack of insulin
  • hypokalaemia is an indicator of severe DKA
  • may show hypomagnesaemia and hypophosphataemia
17
Q

What investigation is done if severe DKA?

A

ECG - MI, hypokalaemia (U waves) or hyperkalaemia (peaked T waves)

18
Q

How does alcoholic ketoacidosis present differently to DKA and how is it managed? (1 + 2)

A
  • low or normal glucose levels (vs high)
  • rehydration with IV saline 0.9%
  • thiamine to prevent Wernicke’s encephalopathy
19
Q

What are some differential diagnoses for DKA? (7)

A
  • hyperosmolar hyperglycaemic state (T2DM, glucose>33.3mmol/L, normal urine ketones)
  • lactic acidosis (normal serum glucose and ketones, elevated serum lactate)
  • starvation ketosis
  • alcoholic ketoacidosis (occurs when alcohol and caloric intake decreases)
  • salicylate poisoning
  • ethylene glycol/methanol intoxication
  • uraemic acidosis
20
Q

What is the diagnostic criteria for DKA? (4)

A

All 4 needed:

  • acidaemia (pH<7.3)
  • hyperglycaemia (>11mmol/L)
  • ketonemia (>3mmol/L)
  • bicarbonate (<15mmol/L)
21
Q

What are the key parts to DKA management?

A
  • fluid replacement
  • insulin (reduce ketones)
  • correction of electrolyte imbalances
22
Q

How do we manage fluid replacement in DKA?

A
  • most patients with DKA deplete around 5-8L
  • isotonic saline used initially, even if patient severely acidotic
  • if SBP<90mmHg - 500ml bolus saline over 10-15min (if no response give second bolus)
  • if SBP>90mmHg / response to first bolus - start 1L 0.9% NaCl over 1 hour
  • add KCl to second litre of IV fluids
23
Q

What do you give if pH<6.9 in DKA?

A

Sodium bicarbonate

24
Q

How do we manage insulin replacement in DKA?

A
  • fixed-rate IV insulin infusion started at 0.1 units/kg/hour (50U soluble insulin in 50mL normal saline)
  • once BGC <15mmol/L, add 10% dextrose
  • if capillary ketones <0.3, pH>7.3 or HCO3>18, use SC insulin instead (however there must be overlap between IV and SC insulin for 1-2h)
25
Q

What do we do with existing insulin medication in DKA?

A

Continue long-acting insulin, stop short-acting insulin

26
Q

How do we correct electrolyte disturbance in DKA?

A
  • serum K+ often high on admission despite total body K+ being low
  • this often falls quickly following treatment with insulin (as insulin drives K+ into cells) –> hypokalaemia –> potassium replacement
  • if the rate of potassium infusion >20mmol/hr, then cardiac monitoring may be required
27
Q

What are the signs of DKA resolution (within 24h), and what do we do if this has not happened? (3 + 1)

A
  • pH>7.3 and
  • ketones <0.6mmol/L or <2+ urine dip and
  • bicarbonate >15mmol/L

If has not resolved: refer to senior endocrinologist

28
Q

What are some complications of DKA itself (not iatrogenic)? (5)

A
  • gastric stasis
  • thromboembolism
  • arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  • ARDS
  • AKI
29
Q

What are some iatrogenic complications from incorrect DKA fluid therapy? (3)

A
  • cerebral oedema (children/young adults)
    • headaches
    • reduced consciousness
    • rise in BP
    • seizures
  • hypokalaemia
  • hypoglycaemia

Year 3 (148 decks)

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