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Year 2 Clinical > Diabetes Emergencies and High Glucose States > Flashcards

Diabetes Emergencies and High Glucose States Flashcards

1
Q

Definition of Diabetic Ketoacidosis (DKA)?

A

Disordered metabolic state that occurs in the context of an absolute/relative INSULIN DEFICIENCY accompanied by an increase in the counter-regulatory hormones, e.g: glucagon, adrenaline, cortisol and growth hormone

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2
Q

In which types of diabetes can DKA occur?

A

By definition, can occur in both Type 1 and Type 2 diabetes

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3
Q

Pathophysiology of DKA?

A

Absolute/relative insulin deficiency causes stress hormone activation:

• Increased lipolysis

This causes increased free fatty acids to the liver and increased KETOGENESIS , leading to acidosis

  • Decreased glucose utilisation
  • Increased proteolysis
  • Increased glycogenolysis

These cause hyperglycaemia, leading to glycosuria (causes electrolyte loss and dehydration)

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4
Q

Main problems in DKA?

A

There is an acidosis and a degree of hyperosmolarity (this is larger in HHS)

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5
Q

Consequences of DKA in pregnancy?

A

High risk of fetal loss

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6
Q

Biochemical diagnostic factors in DKA?

A

Ketonaemia >3 mmol/L or significant ketonuria (>2+ on standard urine stick)

Blood glucose >11.0 mmol/L or known diabetes (the BG is high but not too high in DKA)

Bicarbonate <15 mmol/L or venous pH <7.3

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7
Q

Common precipitants of DKA?

A
  • Infection
  • Illicit drugs and alcohol
  • Non-adherence with treatment (majority)
  • Newly diagnosed diabetes
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8
Q

Types of symptoms and signs of DKA?

A

Osmotic-related

Ketone-body raised

Assoc. conditions

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9
Q

Osmotic-related symptoms in DKA?

A

Polyuria and polydipsia

Dehydration

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10
Q

Symptoms of raised ketone bodies in DKA?

A
  • Flushed
  • Vomiting
  • Abdominal pain and tenderness
  • Breathless (Kussmaul’s respiration as they try to correct acidosis)
  • Ketone body smell on breath (not everyone can smell these)
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11
Q

Conditions assoc. with DKA?

A

Underlying sepsis

Gatroenteritis

True coma virtually never occurs

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12
Q

What is euglycaemic DKA?

A

DKA that occurs at lower than expected or even normal blood glucose levels

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13
Q

Classic glucose levels at DKA presentation?

A

Median level around 40 mmol/L (normal in a non-diabetic is <6 mmol/L)

This can vary from 10 (e.g: in euglycaemic ketosis) to 100 mmol/L

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14
Q

Classic potassium levels at DKA presentation?

A

Usually raised to > 5.5 mmol/l; be more wary of the low normal than a high level

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15
Q

Classic creatinine at DKA presentation?

A

Often raised

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16
Q

Classic sodium levels at DKA presentation?

A

Often reduced

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17
Q

Classic lactate levels at DKA presentation?

A

Raised lactate is very common

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18
Q

Classic blood ketones at DKA presentation?

A

Usually raised to >5:

  • Blood measure - β-hydroxybutyrate
  • Urine measure (obsolete) - acetoacetate
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19
Q

Other biochemistry at DKA presentation?

A

Bicarbonate (<10 in the most severe cases)

Amylase is frequently raised but this does not always indicate pancreatitis (can be salivary in origin)

WCC (if it is raised, it does not always indicate infection)

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20
Q

How much fluid loss can occur in DKA?

A

Variable but can lose up to 12 litres (even higher in HHS)

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21
Q

Risks in DKA to consider?

A

If the person is semi-conscious, is there an aspiration risk? (consider an NG tube)

Is potassium concerning?

Could the patient be septic?

What is the thromboembolic risk?

22
Q

Complications of DKA in adults?

A

Hypokalaemia (can cause cardiac arrest)

Aspiration pneumonia

ARDS (can be a consequence of DKA treatment)

Gastric dilatation

Co-morbidities

23
Q

Complications of DKA in children?

A

Cerebral oedema (tends not to occur in adults)

24
Q

Principles of Mx of DKA?

A

Replace losses:

  • Fluid - initially with 0.9% NaCl; once glucose falls to 15, switch to dextrose
  • Insulin
  • Potassium
  • Phosphate (rarely and bicarbonate (almost never replaced as this would drive more K+ into cells)

Address risks:

  • NG tube, if required, to reduce aspiration risk
  • Monitor K+
  • Prescribe prophylactic LMWH
  • If there is sepsis, find the cause (do a CXR, blood culture, etc)
25
Q

How does insulin deficiency cause DKA?

A

This switches metabolic balance in a catabolic direction

Liver produces glucose via gluconeogenesis and glycogenolysis; fat in adipose tissue is reduced to triglycerides and fatty acids, by lipolysis, and muscle is degraded to release protein (for gluconeogenesis)

Ketone body levels rise, as does the glucose levels which:

  • Increases urine production as it passes the renal threshold (osmotic diuresis)
  • Increased losses of electrolytes via urine • Metabolic acidosis
26
Q

What is Kussmaul respiration?

A

Involuntary attempt to remove CO2 from the blood that would otherwise form carbonic acid and further worsen ketoacidosis

27
Q

Methods of monitoring ketones?

A

Blood ketone testing (using optium meter) - measures β-hydroxybutyrate (<0.6 mmol/l is normal)

Urine ketone testing - measures acetoacetate and this indicates levels of ketones 2-4 hours prior

28
Q

Limitations of urine ketone testing?

A

Ketonuria persists after clinical improvement, due to mobilisation of ketones from fat tissues

29
Q

When is hospital admission indicated in T1DM?

A
  • Inability to tolerate oral fluids
  • Persistent vomiting
  • Persistent hyperglycaemia
  • Persistent +ve/increasing levels of ketones
  • Abdominal pain/breathlessness
30
Q

What is Hyperglycaemic Hyperosmolar Syndrome (HHS)?

A

Hyperglycaemic causes severe dehydration, increases in osmolarity and a high risk of complications, coma and death; diagnosed on features of:

  1. Hypovolaemia
  2. Marked hyperglycaemia (without significant ketonaemia or acidosis)
  3. Osmolarity

It is less common than DKA but the two may present as a mixed picture

31
Q

Typical features of HHS?

A

Diabetes can be known but is often not; if it is known, the the treatment is DIET ALONE, i.e: they are not taking drugs for it

Tends to occur in older individuals; for younger patients, it tends to be in non-Caucasian groups

High refined CHO (carbs) intake pre-event

32
Q

Risk assoc. with HHS?

A

CV event, e.g: stroke or MI

Sepsis

Drugs like glucocorticoids and thiazide diuretics

33
Q

Typical biochemistry in HSS?

A
  • Higher glucose than in DKA (~60)
  • Significantly elevated osmolarity
  • Significant renal impairment
  • Na+ may be raised
  • Less ketonaemic/acidotic than in DKA
34
Q

How to calculate osmolarity?

A

Osmolarity = 2 x (Na + K) + Urea + Glucose

35
Q

Normal osmolarity?

A

285 to 295

36
Q

Compare DKA and HHS?

A
37
Q

Differences in treatment of HHS compared to DKA?

A
  1. Fluids - used more cautiously as there is a higher risk of fluid overload
  2. Insulin - used slowly as more sensitive; they may not require any insulin
  3. Sodium - avoid rapid fluctuations; may consider 0.45% saline (this is halved)
  4. Co-morbidities more likely - screen for vascular events and sepsis; LMWH is given to all unless contraindicated
38
Q

Principles of management of HHS?

A
  1. Measure/calculate osmolarity frequently
  2. Assess dehydration severity and use 0.9% saline for fluid replacement WITHOUT insulin (lowers BG to reduce osmolarity)
  3. Monitory and chart BG, osmolarity and sodium
  4. Start low dose IV insulin only if significant ketonaemia or ketonuria at presentation OR if BG is falling
  5. Assess for complications of therapy, e.g: fluid overload, cerebral oedema
  6. Commence prophylactic anticoagulation
  7. Identify underlying precipitants, e.g: sepsis, and treat
  8. Protect heels and check for foot ulcerations daily (CPR for feet)
39
Q

Production and clearance of lactose?

A

Originates from rbcs, skeletal muscle, brain and renal medulla; it is the end-product of anaerobic metabolism of glucose

Clearance requires hepatic uptake and aerobic conversion to pyruvate then glucose

40
Q

Problems with diagnosing lactic acidosis?

A

Distinguish between hyperlactataemia and lactic acidosis

41
Q

Normal range of lactate?

A

0.6-1.2 mmol/L; once >5 mmol/L, lactic acidosis starts to develop

42
Q

Variability in lactate levels?

A

Lowest in fasting state In severe exercise, can rise 10 mmol/L

43
Q

Types of lactic acidosis and causes of each type?

A

Type A (majority) - assoc. with tissue hypoxaemia:

  • Infarcted tissue, e.g: ischaemic bowel
  • Cardiogenic shock
  • Hypovolaemic shock, e.g: in sepsis (endotoxic shock), haemorrhage

Type B (rare) - may occur in:

  • Liver disease
  • Leukaemic state
  • Assoc. with diabetes, e.g: metformin, severe illness or renal failure
  • Rare, inherited metabolic conditions if they are well and non-diabetic
44
Q

Symptoms and signs of lactic acidosis?

A

Hyperventilation

Mental confusion

If severe, stupor or coma

45
Q

Biochemistry findings in lactic acidosis?

A

Reduced bicarbonate

Raised anion gap

Variable glucose (often raised)

Absence of ketonaemia

Raised phosphate

46
Q

What is the ion gap?

A

[Na + K] - [HCO3 + Cl): normal range is 10-18 mmol/L

-vely charged proteins, sulphate, phosphate and some organic acids make up the difference

47
Q

Uses of the ion gap?

A

Determining the cause of an acidosis, i.e: conditions with a normal anion gap and those with a high anion gap

48
Q

Other causes of lactic acidosis?

A
  • DKA
  • Starvation
  • Uraemia
  • Alcohol, ethylene glycol, methol, salicylate (aspirin) or paraldehyde poisoning
49
Q

Treatment of lactic acidosis?

A

Treat underlying conditions with fluids and/or antibiotics

Withdraw offending medications

Can also give high-dose vitamins

50
Q

Summary of the different metabolic emergencies:

  • Glucose
  • Ketones
  • Dehydration
  • pH
  • SOsm ?
A
51
Q
A

Year 2 Clinical (119 decks)

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