Acute Complications of Diabetes Mellitus Flashcards

1
Q

What are the diabetic emergencies?

A
  • Hypoglycaemia
  • Diabetic ketoacidosis= T1
  • Hyperosmolar Hyperglycaemic Syndrome (HONK)= T2
  • Lactic acidosis (metformin)
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2
Q

Describe hypoglycaemia

A
  • Commonest diabetic emergency
  • Most episodes treated at home
  • Average person with Type 1 DM will experience 1000s of episodes of mild hypoglycaemia
  • 1-2 episodes of severe hypoglycaemia every year (very variable)
  • Severe = need for external assistance
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3
Q

What are the common causes of hypoglycaemia?

A
-Patient error- 
=too much insulin
=too little carbohydrate
=Missed/late meal
=Exercise
-Alcohol
-(Same applies for patients on sulphonyreas eg gliclazide, glipizide= stimulates body to make insulin)
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4
Q

What are the mechanisms of sulfonylureas?

A
  • Encourage beta cells to produce more insulin, close potassium ATPase channel without glucose
  • Glucose entering cell by GLUT2, broken down by glycolysis, mitochondria use to make ATP, powers K-ATPase channel, depolarisation, influx of calcium, triggers release of insulin
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5
Q

What are the less common causes of hypoglycaemia?

A
  • Decreased insulin requirements e.g. weight loss (fat resistant to insulin)
  • Liver disease, alcohol (glucagon on liver activity decreases)

-Conditions associated with T1DM (autoimmune)
=Coeliac disease (less absorption of carbohydrate)
=Addison’s disease (cortisol important in counter regulation)
=Hypothyroidism (slows basal metabolic rate)
=(Hypopituitarism)

-Complications of diabetes
=Autonomic neuropathy (damage to nerves that control automatic processes, gastroparesis or rapid transit time in bowel= less absorption)
=Injection sites/lipohypertrophy
=Renal failure (excretes insulin less efficiently)
=Counterregulatory failure

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6
Q

Describe counter regulation of hypoglycaemia

A

SHORT TERM (drops below 4)
-Glucagon= alpha cells in pancreas, balances insulin (when blood sugar is low)
-Epinephrine/ adrenaline= adrenal gland
=heart racing
=sweaty
=shaky
=EEH impaired, brain not working so well (3 mmol)
=Cognitive function decline (2,8)
=impaired consciousness, coma, death/ severe neuroglycopenia (less than 1.5)

LONGER TERM

  • Cortisol= adrenal gland, protective hormone in prolonged hypoglycaemia
  • GH= pituitary
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7
Q

What are the symptoms of hypoglycaemia?

A
-Autonomic
=Sweating
=Shaking
=Palpitations
=Hunger
-Neuroglycopenic
=Confusion
=Irritable
=Anxious
=Drowsiness
=Blurry vision
=Difficulty speaking
=Odd behaviour
=Incoordination
-Malaise
=Nausea
=Headache
=Weakness/ fatigue
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8
Q

How to symptoms of hypoglycaemia change with age and time?

A
  • These are most common symptoms in young adults
  • Children often manifest behavioural change
  • Elderly can have neurological symptoms (eg mimic stroke)
  • Symptoms are idiosyncratic and may change with time
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9
Q

Why might symptoms of hypoglycaemia change over time?

A

-Counter-regulatory hormones change over time
=lost ability to produce as a result of hypoglycaemia
=Glucagon response first
=Adrenaline
=Cortisol
=Growth Hormone
Therefore Impaired Awareness of Hypoglycaemic (gradually at lower blood sugar levels therefore reduces ability to help themselves)

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10
Q

How is impaired awareness of hypoglycaemia a cycle?

A

-Hypoglycaemia
=Impaired physiological responses to hypoglycaemia (less response, less warnings)
=Reduced awareness of hypoglycaemia
=Increased vulnerability to further episodes of hypoglycaemia

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11
Q

How do we diagnose hypoglycaemia?

A

-Whipple’s triad: 2 out of 3 of-
=Typical symptoms
=Biochemical confirmation (no agreed cut-off, blood glucose level- usually 4 mmol/L, above level of counter-regulatory hormones and safety buffer)
=Symptoms resolve with carbohydrate
-Remember ‘atypical’ presentations esp in elderly
=Hemiparesis
-In theory, confirm with laboratory blood glucose – but don’t delay treatment

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12
Q

How is hypoglycaemia managed?

A
  • If alert, give sweet drink or dextrose tablet
  • If not alert give 20% dextrose iv (or Hypostop, Polycal gels, buccal)= may aspirate into lungs if oral
  • If can’t get iv access, give 1mg intramuscular glucagon plus sweet drink (not effective in alcoholic hypo)
  • Follow-up rapid acting carbs with slow release carbs (toast, digestive biscuits)
  • 10% glucose infusion if long-acting insulin or SU.
  • If recovery not rapid (5-10 minutes), consider other cause.
  • Full cognitive recovery can lag by 45 mins (driving)
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13
Q

How has sugar tax affected hypoglycaemia management?

A
  • Glucose content of carbonated soft drinks is being reduced
  • This is as a result of a levy on sugary drinks
  • Some companies have publicised the change – others will not

=We no longer routinely recommend drinks like Lucozade to treat hypos
=Tea with sugar or fruit juice still fine

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14
Q

Describe the aftercare of hypoglycaemia

A

-Follow-up glucagon/ dextrose with a starchy snack
-Patients presenting to hospital with hypo are
=Older
=Live alone
=Co-morbidity
=Sulfonylurea therapy
-Discharge if make full recovery and responsible adult at home – but not if sulfonylurea-induced
-Inform the diabetes team
-Close monitoring of blood glucose for next 72 hours
-Was there an obvious remedial cause?
-If not, cut right back on insulin doses

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15
Q

Describe continuous subcutaneous glucose sensors

A
  • Worn in skin
  • Bluetooth readings to device on belt
  • Continuous view of blood sugars
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16
Q

How does hypoglycaemia affect driving?

A

-DVLA issues advice letter to drivers on hyopglycaemia

-Drivers with insulin-treated diabetes should:
=Carry glc meter and rescue carbohydrate
=Check glc before driving (even short journeys)
=Test every 2h on long journeys. Regular snacks advised
=If glc is ≤ 5mmol/l, take a snack
=If glc ≤4mmol/l, do not drive
=Carry ID saying you have diabetes in case of accident

17
Q

What do you have to do if you have a hypo while driving?

A
  • Stop vehicle as soon as safe
  • Switch off engine and remove keys from ignition
  • Get out of driver’s seat
  • Wait 45 mins after blood glc normal before driving
18
Q

Who qualifies for extra standards according to the DVLA?

A
  • Group 1 entitlement: car or motorcycle
  • Extra standards for taxi drivers rest with local authority
  • Group 2 entitlement: LGV (large goods vehicle) or PCV (passenger carrying vehicle) Stricter rules
19
Q

What events must drivers inform the DVLA of?

A
  • > 1 severe hypo within last yr (need for assistance)
  • [Grp 2 entitlement must report any severe hypo]
  • If you or your carer feel you are at high risk of developing hypo
  • Develop impaired hypo awareness
  • Suffer hypo while driving
  • Any of the above can result in loss of licence for 1 yr (do not distinguish between illegal drugs and prescribed medication)
  • Risk of hypoglycaemia associated with going onto insulin can have implications for job
20
Q

Describe the pathogenesis of DKA

A

-Profound insulin deficiency
=glucose circulating in system but cells cant use for energy
=free fatty acids converted into ketone bodies (alternative source of fuel)
=acidic so cause metabolic acidosis
=ketones removed from urine
=ketonuria, osmotic diuresis
=hypovolaemia
-Also amino acids produced converted into glucose by gluconeogenesis more osmotic diuresis

21
Q

Describe the pathogenesis of HHS

A

-Hyperosmolar Hyperglycaemic Syndrome
=Excess glucagon
=Break down muscles to produce amino acids (lactate and arginine)
=Gluconeogenesis cycle
=More glucose cant be used
=Remove glucose through urine, sugar creates osmotic diuresis and hypovolaemia
=Reduces GFR

22
Q

What are the principles of management in DKA?

A
  • Fluids: initially fast then slower, to rehydrate
  • iv insulin: switch off ketone body production
  • Monitor potassium: metabolic acidosis shifts K+ to extracellular space. As you give insulin, K+ moves into the cells and K+ falls
  • Protocol driven
  • Seek the precipitant. Commonly infection and errors/omissions (stress response)
  • Often no cause found.
  • In 10% cases, DKA is first presentation of T1DM
  • Try to prevent recurrence
23
Q

How is DKA diagnosed?

A

-Polyuria, polydipsia
-Hypovolaemia
= JVP decreased, decreased BP, increased HR.
= ~5L fluid deficit
= Significant electrolyte deficit Na+ K+ and Cl-)
-Abdo pain, N&V
-Kussmaul resps (respiratory compensation), ketotic breath
-Muscle cramps
-There may be evidence of preciptant (eg sepsis)

24
Q

What is the timeline of DKA?

A
-First hour
=Confirm diagnosis
=Start rapid iv fluids
=Start iv insulin
-1-4 hours
=Review potassium
=Add 10% glucose once blood glucose 14 or less
25
Q

What happens after a DKA event?

A

-Swap to s/c (subcutaneous) insulin once patient eating and drinking
-Ensure basal insulin given ≥ 1h before iv insulin stops
-Try to identify precipitant
-Don’t miss opportunity for pt education
=Sick day rules
=Adjusting insulin
-Involve DSN/dietician, ensure F/U
-Look out for any complications

26
Q

Describe HHS

A
  • Usual finding is MARKED hyperglycaemia (60s and above), raised osmolality and mild/no ketoacidosis (do not present as acute)
  • Mortality up to 33% (age older, precipitant, pre-morbidities)
  • 2/3 cases in previously undiagnosed DM
  • Affects middle-aged or elderly type 2 DM
27
Q

Describe HHS diagnosis

A
  • Hyperglycaemia (>30mmol/l, but often 60-90 mmol/l))
  • Serum osmolality >320mmol/Kg (increased)
  • No / mild ketoacidosis
  • Severe dehydration and pre-renal failure common/ AKI

-Calculated osmolality =2x(Na+K)+glc+urea.

28
Q

How does HHS present?

A
  • Insidious onset (3 days to a week)
  • Profound dehydration (9-10L deficit)
  • Hypercoagulability (exclude CVA, DVT, PE)
  • Confusion, coma, fits.
  • Gastroparesis, N&V, haematemesis
29
Q

Describe HHS management

A
  • Slower, prolonged rehydration (older, underlying heart disease)
  • Gradual reduction in Na+
  • Gentler glucose reduction
  • Anticoagulation vital: Prophylactic subcutaneous heparin
  • Seek the precipitant (infection, MI etc)
30
Q

Describe lactic acidosis and metformin

A

-Metformin is excreted solely through the kidney
-Short t½ so rarely accumulates in absence of advanced RF
-Usually, tissue hypoxia is “trigger” (infection)
=no real evidence causes lactic acidosis

31
Q

What pragmatic suggestions increase safety in metformin?

A

-Stop MF if eGFR <30 (or worsening fast)
-Withdraw during tissue hypoxia but can reinstate later
=‘Shock’
=MI, significant CCF
=Sepsis
=Dehydration
=Acute renal failure
-Withdraw for 3 days after iodine-containing contrast medium given. Check U/E before reinstating 48h later
-Withdraw 2 days before general anaesthetic and reinstate once renal function stable