Acute Complications of Diabetes Mellitus Flashcards
What are the diabetic emergencies?
- Hypoglycaemia
- Diabetic ketoacidosis= T1
- Hyperosmolar Hyperglycaemic Syndrome (HONK)= T2
- Lactic acidosis (metformin)
Describe hypoglycaemia
- 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
What are the common causes of hypoglycaemia?
-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)
What are the mechanisms of sulfonylureas?
- 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
What are the less common causes of hypoglycaemia?
- 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
Describe counter regulation of hypoglycaemia
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
What are the symptoms of hypoglycaemia?
-Autonomic =Sweating =Shaking =Palpitations =Hunger -Neuroglycopenic =Confusion =Irritable =Anxious =Drowsiness =Blurry vision =Difficulty speaking =Odd behaviour =Incoordination -Malaise =Nausea =Headache =Weakness/ fatigue
How to symptoms of hypoglycaemia change with age and time?
- 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
Why might symptoms of hypoglycaemia change over time?
-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)
How is impaired awareness of hypoglycaemia a cycle?
-Hypoglycaemia
=Impaired physiological responses to hypoglycaemia (less response, less warnings)
=Reduced awareness of hypoglycaemia
=Increased vulnerability to further episodes of hypoglycaemia
How do we diagnose hypoglycaemia?
-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
How is hypoglycaemia managed?
- 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)
How has sugar tax affected hypoglycaemia management?
- 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
Describe the aftercare of hypoglycaemia
-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
Describe continuous subcutaneous glucose sensors
- Worn in skin
- Bluetooth readings to device on belt
- Continuous view of blood sugars
How does hypoglycaemia affect driving?
-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
What do you have to do if you have a hypo while driving?
- 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
Who qualifies for extra standards according to the DVLA?
- 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
What events must drivers inform the DVLA of?
- > 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
Describe the pathogenesis of DKA
-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
Describe the pathogenesis of HHS
-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
What are the principles of management in DKA?
- 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
How is DKA diagnosed?
-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)
What is the timeline of DKA?
-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
What happens after a DKA event?
-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
Describe HHS
- 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
Describe HHS diagnosis
- 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.
How does HHS present?
- Insidious onset (3 days to a week)
- Profound dehydration (9-10L deficit)
- Hypercoagulability (exclude CVA, DVT, PE)
- Confusion, coma, fits.
- Gastroparesis, N&V, haematemesis
Describe HHS management
- 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)
Describe lactic acidosis and metformin
-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
What pragmatic suggestions increase safety in metformin?
-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
