Diabetic emergencies Flashcards

1
Q

Define what Diabetic ketoacidosis (DKA) is

A

DKA is a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increase in the counter-regulatory hormones i.e. glucagon, adrenaline, cortisol and growth hormone.

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2
Q

Can DKA occur in both T1DM and T2DM?

A

Yes - but much more common in T1DM

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3
Q

What is most patients who develop DKA’s, glycaemia control like?

A

They usually have poor gylcaemic control

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4
Q

What is the biochemical facotors used to dianose DKA?

A
  • Ketonaemia > 3mmol /L, or significant ketonuria (>2+ on standard urine stick)
  • Blood glucose > 11.0 mmol /L or known diabetes (NB euglycaemic DKA)
  • Bicarbonate < 15 mmol /L or venous pH < 7.3
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5
Q

Describe the pathophysiology of DKA

A
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6
Q

List some of the factors which predispose patients to DKA?

A
  • Infection (20 to 25%) – may be an over-estimate
  • Illicit drugs and alcohol (10 to 15%)
  • Non-adherence with treatment (45 to 50%) – may be under-estimate
  • Newly diagnosed diabetes (25%)
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7
Q

What ages is DKA usually seen in ?

A

Young people but can be older

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8
Q

What are the typical symptoms of DKA?

A

Osmotic related:

  • Thirst and polyuria
  • Dehydration

Ketone body related:

  • Flushed
  • Vomiting
  • Abdominal pain and tenderness
  • Breathless – Kussmaul’s respiration
  • Note - not all individuals can smell ketones on breath
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9
Q

List a couple conditions associated with DKA

A
  • Underlying sepsis
  • Gastroenteritis
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10
Q

List the rest of the biochemical results which suggest DKA

A

Glucose

  • Median level around 40 mmol/L - [Normal<6]P

Potassium

  • Usually raised above 5.5 mmol/L (complications arise due to low K so i think its actually usually low)

Creatinine: often raised

Sodium: often reduced

Raised lactate is very common

Blood ketones usually raised to > 5

  • Blood measure is βhydroxybutarate
  • Urine is acetoacetate

Bicarbonate: <10 in most severe cases

Amylase very frequently raised – does not necessarily mean pancreatitis [can be salivary in origin]

White cell count

  • Median around 25
  • Does not always infer infection
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11
Q

Give examples of some of the complications of DKA

A
  • Low K – cardiac arrest and death
  • Brain swelling another complication
  • Gastric diliatation
  • ARDS
  • Aspiration pneumonia
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12
Q

How is DKA treated ?

A

Fluid: (oral if alert, IV if unconscious)

  • Initially with 0.9% sodium chloride
  • Glucose falls to about 15, switch to dextrose

Give insulin (oral if alert, IV if unconscious)

Potassium replacement if needed

Phosphate is rarley replaced and bicarbonate is almost never replaced

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13
Q

What monitoring tests are done for patients with DKA?

A

Potassium levels monitored

Source sepsis: CXR, Blood Culture, MSSU +/- viral titres, etc.

Prescribe prophylactic LMWH (low molecular weight heparin)

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14
Q

What are the symptoms of diabetes

A
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15
Q

What are the typical features of HHS (hyperglycaemic hyperosmolar syndrome)?

A
  • General: fatigue, lethargy, nausea and vomiting
  • Neurological: altered level of consciousness, headaches, papilloedema, weakness
  • Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
  • Cardiovascular: dehydration, hypotension, tachycardia
  • Usually older individuals with T2DM
  • High refined CHO intake pre-event
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16
Q

List some of the factors which can predispose patients to HHS

A
  • Cardiovascular event [stroke or MI]
  • Sepsis
  • Medications: Glucocorticoids and thiazide diuretics.
17
Q

What is the typical biochemistry in HHS?

A
  • Higher glucose than in DKA -Median around 60
  • Significant renal impairment (high creatinine?, low GFR?)
  • Sodium may be raised
  • Significant elevation of osmolality – often around 400 (norm is around 285-29). Osmolality=2x[Na+K] + Urea + Glucose
  • Less ketonaemic/acidotic as compared to DKA
18
Q

How is HHS diagnosed ?

A
  1. Hypovolaemia
  2. Marked hyperglycaemia >30mmol/L (without significant ketonaemia or acidosis)
  3. Osmolality >320mmol/L
19
Q

What are the principles of management of patients with HHS?

A
  1. Monitor BG, sodium and osmolality every 1-2 hrs to monitor progress
  2. Assess severity of dehydration and give 0.9% saline (+/- K+) for fluid replacement WITHOUT insulin. This alone will lower BG which will reduce osmolality
  3. Start low dose IV insulin (0.05units/kg/hr) if significant ketonaemia or ketonuria present or BG falling at rate lower than 5mmol/hr despite adequate fluid replacement therapy
  4. Commence prophylactic anticoagulation
  5. All at risk of foot ulcers so check regularly and prevent
20
Q

Compare HHS and DKA ?

A

Also LMWH is always given in HHS unless contra-indicated this is not the case in DKA

21
Q

Where does lactate originate from and what is it the product of ?

A

Product of anaerobic metabolism of glucose and originates from red cells, skeletal muscle, brain and renal medulla

22
Q

How is lactate cleared ?

A

Taken up by the liver and converted into pyruvate then glucose by aerobic conversion

23
Q

What is the normal range of lactate ?

A

0.6-1.2 mmol/L

24
Q

What can be a cause of a very high lactate ?

A

Severe exercise

25
Q

This is the ion gap - [Na+ + K+] – [HCO3- + Cl-] what is its normal range ?

A

10-18mmol/L

26
Q

What are the different types of lactic acidosis ?

A

Type A (almost always this type) and Type B

27
Q

What is type A lactic acidosis associated with ?

A

Associated with tissue hypoxaemia

  • Infarcted tissue, eg ischaemic bowel
  • Cardiogenic shock
  • Hypovolaemic shock
  • Sepsis [endotoxic shock]
  • Haemorrhage
28
Q

What is type B lactic acidosis associated with ?

A
  • May occur in liver disease
  • May occur in leukaemic states
  • Associated with diabetes- 10% of cases of DKA associated with lactate >5 mmol/L. With Metformin usually in severe illness states or renal failure
29
Q

What are the clinical features of lactic acidosis ?

A
  • Hyperventilation
  • Mental confusion
  • Stupor or coma if severe
30
Q

What are the lab findings in patients with lactic acidosis ?

A
  • Reduced bicarbonate
  • Raised anion gap [(Na+ + K+) – (HCO3 + Cl-)]
  • Glucose variable – maybe [often] raised
  • Absence of ketonaemia
  • Raised phosphate
31
Q

What is the treatment of lactic acidosis?

A

Treat Underlying condition

  • Fluids
  • Antibiotics (for e.g. sepsis)

Withdraw offending medication

32
Q

Summarise the different biochem findings for the different metabolic emergencies

A