Diabetes Related Emergencies and complications: Flashcards

1
Q

What is Diabetic Keto Acidosis?

A

In response to the absence of insulin:
- Increased glycogenolysis and gluconeogenesis plus reduced glucose uptake by tissues
= hyperglycaemia (>11mmol/L)

  • Increased urine out-put (to remove glucose)= Dehydration
  • Suppressed lipolysis
    = Accumulation of free fatty acids. Metabolised to ketones
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2
Q

Symptoms of DKA?

A

Results in:
- Profound acidosis (pH <7.4 but often <7.0)
- Severe dehydration
- Symptoms:
Tachypnoea (physiological response to acidosis)
Altered mental state (drowsiness or coma)
Nausea, vomiting, abdominal pain

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3
Q

Management of DKA – first 4 hours (Adults and Children)?

A

Fluid resuscitation – first hour

  • Isotonic fluids only (0.9% sodium chloride, Plasmalyte)
  • Given slowly
    • ->Rapid fluid replacement – cerebral oedema, coma and death

Insulin Variable Rate Infusion(1-2hrs after fluid)

  • “Sliding scale” – 0.05 to 0.1unit/kg/hr
  • Monitor capillary blood glucose (cBG) HOURLY
  • Once cBG <15mmol/L consider move to maintenance fluid
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4
Q

Management of DKA – maintenance(Adults)?

A

Maintenance fluid (2L/day maximum)

  • Give glucose containing fluid (0.9% sodium chloride + 5% glucose) WITH potassium chloride
  • Continue insulin “sliding scale”

Once ready to eat and drink
Let patient eat THEN:
- Give sc insulin 30 minutes before stopping insulin infusion THEN:
Stop glucose IV

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5
Q

Management of DKA – maintenance (Children & Young People

A

Fluid restriction 50% “normal maintenance”

  • 10kg = 2ml/kg/hr
  • 10-40kg = 1ml/kg/hr
  • > 40kg = 40ml/hr (not weight based)
Replace fluid deficit (dehydration) over 48hrs
Start s/c insulin when:
- cBG <14mmol/L
- Ketones <3mmol/L
- Resolved acidosis
- Oral fluids tolerated
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6
Q

Complications of DKA:

A
  • Fatality rate ranging from 0.15 percent to 0.31 percent1 in children
  • Cerebral oedema (most common cause of fatality caused by rapid movement of water into cells in the brain)

Signs & Symptoms

  • Bradycardia
  • Dilated pupils
  • Altered mental state/unconsciousness
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7
Q

What Is Hyperosmolar Hyperglycaemic State?

A
  • In response to lack of insulin effect
  • Insulin is still there so NO lipid metabolism
  • Severe hyperglycaemia (BG usually >50 mmol/L) + hyperosmolality (Serum osmolality usually >350mosmol/kg)
  • High blood sugars results in increased urination and dehydration
  • Little to no acidosis
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8
Q

Prevention of DKA?

A

A lot of DKA occurs due to poor understanding of how insulin works in the body
Patients think they only need insulin if they eat
Insulin is required for many normal body processes even when not eating

SICK DAY RULES

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9
Q

Aims of treating DKA?

A

Initially:

  • Normalise osmolality
  • Replace fluids
  • Balance electrolytes

Also Prevent:

  • Clots due to thickened blood and slow flow
  • Foot ulcers
  • Cerebral oedema
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10
Q

Treatment of hyperglycaemia?

A
  • Lots of physiological fluid (not just sodium chloride 0.9%) to correct blood pressure
  • Target SBP >90mmHg
  • Start SLOW variable rate insulin infusion (aim a rate of no faster than 5mmol/l/min
  • Replace potassium as required
  • Give clot preventing medication (Low molecular weight heparins)
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11
Q

How do we avoid hyperglycaemia?

A
  • Early Diagnosis
  • Good glucose control
  • Diabetes education
  • Appropriate monitoring
  • Recognition of symptoms
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12
Q

What is hypoglycaemia?

A

Hypoglycaemia (<4.0mmol/l in people with medication controlled diabetes)

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13
Q

Autonomic symptoms of Hypoglycaemia:

A

Tremor
Sweating
Hunger
Palpitations

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14
Q

Neuroglycopenic symptoms of Hypoglycaemia:

A
  • Odd behaviour, poor co-ordination or confusion
  • Drowsiness/loss of consciousness
  • Visual disturbance
  • Seizures
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15
Q

Non specific symptoms of hypoglycaemia?

A

Headache and nausea

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16
Q

Ways to replace glucose at home?

A

Short acting carbs followed by long acting carbs
At home:
Lucozade /Sweets (other sugary drinks are available)
Meal if due or snack such as biscuits

17
Q

Ways to replace glucose in hospital?

A

If conscious - Dextrose tabs or Glucogel then meal if due or snack such as biscuits
If unconscious - Glucogon IM followed by 10% glucose 100ml/hr

18
Q

What are the two groups of complications?

A

Classified by the blood vessels affected
MICROvascular –small vessels
MACROvascular – large vessels

19
Q

Microvascular Complications include:

A
Diabetic Retinopathy (eyes)
Diabetic Neuropathy (nerves)
Diabetic Nephropathy (kidneys)

No preventative drug treatment

20
Q

What is retinopathy?

A
  • High blood sugar causes micro-thrombi in the retina.
  • The capillaries become blocked
  • Proliferative retinopathy – new vessels form and leak blood into vitreous blocking light entry
  • Non-proliferative retinopathy – no new vessels form
  • No drug treatment – laser therapy
  • Irreversible – leads to blindness
  • Glucose control
  • Yearly optician visits for monitoring
21
Q

What is neuropathy?

A
  • High blood sugars leads to reduced blood flow and death of nerves
  • Most common is peripheral neuropathy
  • Often results in diabetic foot ulcers
  • Regular foot checks
  • Foot clinic
22
Q

Problems with neuropathy treatment:

A

Hard to treat – bacteria love high blood sugars, reduced sensation often means pt not aware. Poor blood flow reults in poor abx penetration and lack of natural immune response

23
Q

Symptom treatment of neuropathy?

A

Anti-depressants -

  • Duloxetine
  • Amitriptyline

Anti-convulsants -

  • Gabapentin
  • Pregabalin

Topical -
- Capsacin based creams/gels

Short term options -
- Tramadol

Avoid -

  • NSAIDS
  • Long-term opiates
24
Q

How do diabetic foot ulcers arise?

A
  • A complication of neuropathy
  • Lack of sensation increases risk of damage to feet
  • High blood sugars increase infection risk and reduce healing
  • Require prolonged antibiotic courses
  • May result in amputations
25
Q

Examples of other neuropathic conditions:

A
  • Gastroparesis (treated with erythromycin, metoclopramide or domperidone)
  • Erectile dysfunction (treated with phosphodiesterase type 5 inhibitors e.g. sildenafil)
  • Diabetic diarrhoea (treated with loperamide)
  • Loss of bladder control
  • Arrhythmias
  • Lack of or excessive sweatin
26
Q

What is nephropathy:

A
  • Linked to poor glucose control and poor blood pressure control
  • Nephrons become thickened and scarred so less effective
  • Kidney function becomes progressively worse
  • Diabetes is the most common reason for patients requiring dialysis
27
Q

Treatment of nephropathy?

A
  • Good control of blood pressure

- Ideally with an ACE or ARB

28
Q

Name some microvascular complications:

A
  • High insulin levels are associated with atherosclerosis
  • Diabetes related dyslipidaemia also speeds up the atherosclerotic process

Result:

  • Myocardial infarctions
  • Ischaemic Strokes
  • Vascular disease
29
Q

Prevention of microvascular complications:

A
  • Control of cholesterol
  • Control of blood pressure

If evidence of cardiovascular disease:
Consider aspirin 75mg OD (NOT for primary prevention)

  • Control of blood sugars!
30
Q

Blood pressure treatment?

A
Targets:
140/80 mmHg
Treatment:
- Start with ACE inhibitor (or ARB if cough)
- Then add CCB or thiazide like diuretic

Beta blockers not used as they mask symptoms of diabetes

31
Q

Cholesterol control and treatment:

A
Offer atorvastatin 20mg to:
Type 1
- older than40 yearsor
- had diabetes for more than10 yearsor
- have established nephropathyor other cardiovascular disease risk factors.

Type 2
- who have a 10% risk or greater of developing cardiovascular disease in 10 years using QRISK scoring

Aim to reduce HDL by 40% in 3 months – titrate dose to achieve this