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Stage 2: Inflammation > Diabetes Emergencies - DKA and HHS > Flashcards

Diabetes Emergencies - DKA and HHS Flashcards

1
Q

What are the 3 diabetic emergencies?

A

1) DKA
2) Hyperosmolar hyperglycaemic state (HHS)
3) Severe hypoglycaemia

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2
Q

What is DKA?

A

A complex disordered metabolic state due to absolute or relative insulin deficiency
- Rapid onset < 24h

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3
Q

In what type of patients does DKA mainly occur?

A

T1D

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4
Q

What are the three features that define DKA?

A

1) Hyperglycaemia
2) Hyperketonaemia
3) Metabolic acidosis

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5
Q

What are the three diagnostic criteria for DKA?

A

1) Blood glucose > 11 mmol/l (or known diabetes)
2) Blood ketones ≥ 3 mmol/l or ketonuria > 2+
3) Bicarbonate < 15 mmol/l and/or venous pH < 7.3

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6
Q

Why does DKA occur?

A
  • No insulin action
  • Uncontrolled production of glucose and ketones and no glucose is taken up into cells
  • Dehydration and disordered potassium promotes stress hormone production as well as physiological stress which increases glucose and ketone production even more by the liver
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7
Q

What does insulin do to potassium?

A

Causes it to move into cells

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8
Q

What happens to potassium in DKA?

A

1) Insulin deficiency
2) K leaks out of cells
3) High extracellular K
4) Hyperkalaemia
5) Renal K loss
6) Whole body K depletion

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9
Q

What is the effect of acidosis on potassium?

A

Reduces intracellular potassium bc H+ and K+ compete

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10
Q

What happens to potassium when DKA is treated with insulin?

A

1) K moves rapidly into cells
2) Bc the whole body is K deplete, extracellular/serum K falls very quickly
3) Hypokalaemia - can be just as dangerous

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11
Q

What happens in DKA?

A

1) Insulin deficiency ± increased stress hormones
2) Increased production of glucose (liver) and reduced uptake (muscle/fat) - hyperglycaemia
3) Increased lipolysis (adipose tissue) and release of NEFA
4) NEFAs converted to ketone bodies in liver
5) Acetoacetate and 3-hydroxybutyrate cause acidosis
6) Dehydration due to hyperglycaemia and osmotic diuresis
7) Hyperkalaemia and whole body potassium depletion

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12
Q

What are the precipitating causes of DKA?

A

1) Infection
2) Poor compliance
3) Newly diagnosed
4) Failure of care

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13
Q

What are complications of DKA?

A

1) Cerebral oedema - decrease consciousness (due to changes in fluid shifts, can be made worse by IV fluids in treatment)
2) Adult respiratory distress syndrome or acute lung injury
3) PE
4) Arrhythmias
5) Multi-organ failure (acidosis)
6) Co-morbid states

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14
Q

What are the symptoms of DKA due to?

A

Dehydration and acidosis

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15
Q

What are symptoms of DKA?

A
  • Polyuria, polydipsia, thirst
  • Weight loss
  • Blurred vision
  • Vomiting
  • Abdominal pain
  • Weakness
  • Leg cramps
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16
Q

What are the signs of DKA?

A
  • Kussmaul breathing
  • Ketotic fetor (sweet nail varnish smell)
  • Dehydration
  • Tachycardia
  • Hypotension
  • Mild hypothermia
  • Confusion, drowsiness, coma
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17
Q

What 3 bedside tests are used to diagnose DKA?

A

1) Capillary blood glucose
2) Blood/urine ketones
3) Venous blood gases
4) GCS

18
Q

What other investigations are used to look for complications or precipitants of DKA?

A
  • Lab Glucose
  • Bloods - U&Es, FBC, CRP
  • ECG
  • CXR
  • Blood culture
  • MSU
19
Q

What are the two aims of DKA treatment?

A

1) To clear the ketonaemia and metabolic acidosis (NOT hyperglycaemia)
2) Avoid complications of DKA and its management

20
Q

How do you treat DKA?

A

1) Fluid replacement
2) Insulin replacement
3) Potassium replacement
4) Identify and treat the cause
5) VTE prophylaxis
6) Monitor (HDU)

21
Q

How do you give fluid replacement in DKA?

A
  • IV 0.9% (normal) saline
  • As soon as you start replacing fluid, you increase the circulating volume and blood flow to kidneys which sort out the metabolic acidosis
22
Q

How do you give insulin replacement in DKA?

A

Fixed rate IV insulin infusion (0.1 units/kg/hour)

23
Q

How do you give potassium replacement in DKA?

A
  • The serum K is high but the total body K is low
  • Once fluid and insulin treatment is started serum K falls rapidly
  • Therefore need to monitor the serum potassium and start replacing K as soon as it is in the normal range
24
Q

What is HHS?

A
  • A state of severe uncontrolled diabetes
  • There is enough insulin to suppress ketogenesis but not enough to suppress uncontrolled glucose production by the liver or promote uptake by cells
  • Develops over days and more severe metabolic disturbance than DKA
25
Q

In what type of patient does HHS occur?

A

T2D

26
Q

What are the characteristics of HHS?

A

1) Hypovolaemia/dehydration
2) Marked hyperglycaemia > 30 mmol/l
3) Hyperosmolarity > 320 mosmol/kg
4) No significant ketonaemia (blood < 3 mmol/l, urine trace) or acidosis (pH > 7.5, bicarbonate > 15 mmol/l)

27
Q

What is it if you have features of HHS + ketones and acidosis?

A

Mixed DKA + HHS

28
Q

Why does HHS occur?

A
  • Profound dehydration causes stress hormones which increase glucose production
  • Often people who don’t have control over when they drink e.g. in nursing homes who can’t communicate
  • Or people who drink sugary drinks when they are thirsty
  • If are extremely thirsty and then drink water can prevent HHS
29
Q

What are precipitating factors of HHS?

A

1) Infection
2) New onset diabetes
3) Acute illness
4) Non compliance

30
Q

What are the complications of HHS?

A
  • Cerebral oedema
  • Osmotic demyelination syndrome (pontine myelinolysis) + neurological damage due to changes in osmolality during development/treatment of HHS
  • Seizures
  • Arterial thrombosis MI, CVA, peripheral arterial (dehydration)
  • VTE/PE
  • Multi-organ failure
  • Foot ulceration bc of prolonged immobility and other diabetic complications
  • Co-morbid condition
31
Q

What are (osmotic) symptoms of HHS?

A
  • Thirst
  • Polyuria
  • Blurred vision
  • Weakness
32
Q

What are the signs of HHS due to profound dehydration?

A
  • Dehydration
  • Tachycardia
  • Hypotension
  • Confusion and drowsiness
  • Coma
33
Q

What bedside tests can you do for HHS?

A

1) Capillary blood glucose
2) Blood ketones
3) Urine ketones
4) Venous blood gases

34
Q

What lab investigations can you do for HHS?

A

1) Glucose
2) Bloods - U&Es, FBC, CRP
3) ECG
4) CXR
5) Blood culture
6) MSU

35
Q

What are the aims of HHS treatment?

A

1) Gradually and safely normalise osmolality, fluid status and glucose (need to do slowly bc body adapts to high osmolality)
- If suddenly bring it down from 360 to 290 over a few hours (too quick) water moves into brain cells, brain swelling, loss of consciousness
2) Avoid complications of HHS and treatment

36
Q

How do you treat HHS?

A

1) Fluid replacement
2) Insulin replacement
3) Identify and treat the cause
4) VTE prophylaxis - LMWH
5) Monitor (HDU or acute medical unit bc can get worse with treatment

37
Q

How do you give fluid replacement in HHS?

A

IV 0.9% (normal) saline

38
Q

How do you give insulin replacement in HHS?

A

Fixed rate IV insulin infusion (lower than for DKA - 0.05 units/kg/hour)

39
Q

What would you do after the diabetic emergency has occurred?

A
  • Find out the cause
  • Can it be prevented?
  • Does the day to day diabetes management need changing?
  • Needs to see diabetes specialist nurse/doctor
40
Q

What is one of the main reasons that people with T1D get DKA?

A

They stop taking their insulin when they are ill bc they are not eating and aren’t bothered to check their blood glucose

41
Q

What should T1D patients do when they are sick?

A
  • NEVER stop background/ long-acting insulin even if vomiting
  • Check capillary blood glucose even more frequently (2-4h)
  • Check for ketones
  • Take extra short acting insulin if CBG > 13 mmol/l or if blood ketones > 1.5 mmol/l
  • Keep drinking fluid (100ml/hour)
  • Bolus for carbohydrate
  • Get medical help if vomiting/diarrhoea, CBG not improving/ketones persist or troublesome hypos

Stage 2: Inflammation (39 decks)

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