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Diabetes and Endocrinology YR3 > Diabetic emergencies > Flashcards

Diabetic emergencies Flashcards

1
Q

Role of insulin

A
  • Transports glucose into muscle, adipose and liver
  • Inhibits lipolysis
  • ANABOLIC
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2
Q

What happens in absence of insulin?

A
  • Glucose accumulates in blood
  • Liver uses amino acids for gluconeogenesis and converts fatty acids into ketone bodies
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3
Q

Ketone bodies examples

A
  • Acetone
  • Acetoacetate
  • B-hydroxybutyrate
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4
Q

Precipitating factors for DKA

A
  • Failure to take insulin - most common
  • Failure to increase insulin
  • Illness/infection - pneumonia, MI, stroke
  • Acute stress - trauma, emotional
  • Medical stress - counterregulatory hormones oppose insulin and stimulate glucagon release
  • Hypovolaemia - increase catacholamines and glucagon, decreased renal blood flow so decreased glucagon degradation by kidneys
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5
Q

DKA presentation

A
  • Polyuria, polydipsia
  • Dehydration - tachycardia, orthostatic hypotension
  • Abdominal pain - N+V
  • Fruity breath - acetone
  • Mental state changes - agitation, drunk like state, coma
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6
Q

DKA biochemical criteria

A

Diabetic:
* Hyperglycaemia BG more than 11mmol/L

Keto:
* Ketonaemia more than 3mmol/L or ketouria

Acidosis:
* Raised anion gap acidosis (more than 12)
* pH less than 7.3

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7
Q

When is glucose sometimes normal in DKA?

A
  • Pregnancy
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8
Q

Treatment of DKA - aims

A
  • Reduce ketones by 0.5/hr
  • Increase HCO3 by 3/hr
  • Reduce glucose by 3/hr
  • Maintain K+ between 4.5-5.5mmol/L (insulin causes hypokalaemia)
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9
Q

Initial assessment for DKA

A
  • Fluid resucitation - 1st
  • Clinical exam
  • Investigation to find cause - VBG, U&E, FBC, ECG, CXR, MCU
  • Cardiac monitoring
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10
Q

Prophylaxis for DKA

A

LMWH - hypercoagulable state

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11
Q

Management of DKA

A
  1. Fluid resucitation
  2. Potassium replacement
  3. Fixed rate insulin infusion
  4. Continious monitoring
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12
Q

Fluid resucitation in DKA

A
  • 0.9% saline 1L over 1hr
  • Then 1L over 2hrs, and another of these
  • Then 1L over 4 hours and another of these

Be more cautious in fluid overload eg CHF

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13
Q

When to check blood gas to check K+ and pH DKA?

A
  • Every time change fluid bag
  • So at 1hr, then 2hr, then 2hr, then 4hr then 4hr
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14
Q

Potassium replacement guide for DKA

A
  • If K+ is more than 5.5 - no replacement
  • If 3.5-5.5 give 40mmol/L
  • If less than 3.5 - additional K+ is needed, consider ITU/HDU
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15
Q

Insulin infusion regime for DKA

A
  • Fixed rate insulin infusion of 0.1unit/kg/hr
  • eg 50 units of Actrapid in 50ml 0.9% saline)
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16
Q

When to cheeck potassium and glucose DKA?

A

Every hour

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17
Q

What does continious monitoring involve in DKA?

A
  • Ensure metabolic targets in aims are achieved
  • Treat underlying cause
  • NG tube or catheter if needed
  • Monitor urine output
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18
Q

Risks with DKA treatment

A
  • Hypoglycaemia - if happens continue insulin but give dextrose
  • Pulmonary oedema - give diuretic
19
Q

When is DKA defined as resolved?

A
  • Ketones less than 0.6mmol/L
  • Bicarbonate more than 15mmol/L
  • pH more than 7.3
  • Ketonaemia and acidosis should resolve within 24hrs - if not need to consult endo
20
Q

What to do once DKA resolved?

A
  • Move to sliding scale/variable regime for overnight/few hours
  • Then re-start previous regime or calculate new if new presentation
  • Most adults need 0.5 units/kg/day
  • Adolescents or high insulin resisatnce 0.8-1 units/kg/day
  • 50% long acting and 50% short acting
  • Short acting split between 3 meals
21
Q

Complications of DKA

A
  • Infection - precipitates DKA, leukocytosis can be secondary to acidosis
  • Shock - if no improvement with fluids
  • Vascular thrombosis - dehydration, cerebral vessels, hours to days after DKA
  • Pulmonary oedema
  • Cerebral oedema
22
Q

Cerebral oedema manageemtn

A
  • Occurs within 24hrs of treatment
  • Mental status changes
  • Mannitol
  • May need intubation and ventilation
23
Q

Who does hyperosmolar hyperglycaemic state often happen in?

A

T2DM elderly pts

24
Q

Why is mortality higher in HHS than DKA?

A
  • Happens in eldery
  • Decreased physiological reserve
  • Mortality higher maybe due to underlying cause precipitating HHS rather than itself
25
Q

What is HHS?

A
  • Extreme hyperglycaemia and dehydration
  • Unable to excrete glucose as fast as it enters extracellular space
  • Hyperglycaemia leads to osmotic diuresis and loss of water (more than electrolytes)
26
Q

Criteria for HHS

A
  • Hypovolaemia
  • Hyperglycaemia - 30mmol/L or more
  • No significant ketonaemia (less than 3 or acidosis pH more than 7.3, HCO3 more than 15mmol/L)
  • High osmolality (more than 320mmol/kg, normal 275-295)
27
Q

Who are at risk of HHS?

A

Elderly patients with illness
Impaired ability to ingest fluids

28
Q

Presentation of HHS

A
  • Decreased urine output
  • Elevated glucose
  • CNS dysfunction
  • Sometimes mixed picture with DKA - treat as if DKA
29
Q

Treatment aims for HHS

A
  • Normalise osmolality and glucose
  • Replace fluid and electrolyte losses
  • Reduce osmolality by 3/hr
  • Reduce glucose by 3-5/hr
  • Achieve +ve fluid balance of 3-6 litres by 12 hours, remaining should be within 12hrs
  • Complete normalisation may take up to 72hrs
30
Q

Initial assessment HHS

A
  • Fluid resuciation
  • Clinical exam
  • Investigation - VBG, U&E, FBC, ECG, CXR, MSU - find cause
  • Cardiac monitoring
31
Q

Prophylaxis for HHS

A

LMWH - increased risk of VTE

32
Q

Fluids in HHS

A

IV 0.9% saline 1L over 1hr
Consider more rapid if systolic is below 90

33
Q

When to caution with fluid treatment in HHS?

A
  • Elderly - rapid replacement may precipitate HF
  • But insufficient can lead to acute kidney injury
34
Q

When to use insulin in HHS?

A

No unless:
* Significant ketonaemia (more than 1mmol/L)
* OR ketonuria of 2 or more
* RATE is slower infusion at 0.05 units/kg/hr

35
Q

Main treatment for HHS?

A

FLUIDS - normalise osmolality

36
Q

Mechanisms of hypoglycaemia

A
  • Medication induced
  • Starvation
  • Insulinoma
  • Reactive hypoglycaemia - mismatch between body insulin production and food
37
Q

Risk factors for hypoglycaemia

A
  • Old age
  • Malnutrition
  • Acute illness
  • Hypoglycaemia unawareness
  • Dementia
  • LOTS
38
Q

What is hypoglycaemia unawareness?

A
  • Pts who have good control of diabetes eg between 4-5 usually
  • Body stops producing symptoms when hypoglycaemia occurs
  • Get silent hypoglycaemia
  • Can then suddenly get syncope
  • Often need CGM and alarm when drops
39
Q

What level is hypoglycaemia?

A

Less than 4mmol/L
Usually 2-4 get sympathetic symptoms
Less than 2 get neurological symptoms

40
Q

Emergency treatment for conscious patient with hypoglycaemia

A
  • 1 glass lucozade (120mls)
  • 150-200mls pure fruit juice
  • 3 dextrosol tablets
  • 1 tube glucose ge;
  • 60mls fortijuice

Treatment may need repeating 5-10 mins after if no improvement
If remains less 4 after 3 attempts or 45 minutes condier glucagon or IV glucose

41
Q

Emergency treatment for patient who is confused/disorientated and unable to tolerate oral treatment hypoglycaemia

A
  • Glucagon - 1mg with dilutents IM

If patient remains uncoperative, usually respond within 10 mins
N+V can occur post dose
If no response (still less than 4) use IV glucose regime

42
Q

Steps to follow if patient unconscious, fitting and unable to swallow

A
  • DO regime for unconcious patient as mentioned in previous card
  • Also check ABC
  • Stop any IV insulin
  • 10% glucose infusion 200ms over 10 mins
  • OR 20% glucose 100mls stat

Usually responds within 4-6 mins
Always check glucose levels 10-15 mins after initial treatment and at 1 hr

43
Q

Management of hypoglycaemia on recovery

A

Longer acting carbohydrate or next meal if due eg:
* sandwhich
* 2 digestives
* 1 slice toast
* non sugary cereals
* 200-300mls milk

44
Q
A

Diabetes and Endocrinology YR3 (28 decks)

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