Complications of Diabetes

Complications of Diabetes
Dr Shanti Vijayaraghavan,
Consultant Diabetologist, Barts Health,
London
15 May 2015
Acute or Short-term Complications
1. Hypoglycaemia: low blood glucose level
2. Hyperglycaemia:
Diabetic Ketoacidosis (DKA)
Hyperosmolar Hyperglycaemic State (HHS)
CB, 32/F
Primary school teacher, type 1 DM of 14 years duration
(
autoimmune)
September 2014
: 
Change of job - desk-based to more active job
Started cycling to work
Sensible diet and plenty of exercise
BMI 23, on Novorapid insulin with each meal, and glargine insulin
at night
January 2015: Very erratic blood glucose control with frequent
hypoglycaemia during the day (upto 10/day)
No hypoglycaemia awareness
March 2015: In a school meeting pre-lunch
Sudden loss of conciousness with ? Seizure
Taken to local A & E
Blood glucose 1.5 mmol/l – requiring IV glucose drips
AC, 82 M
Type 2 diabetes for 30 years
Son reports increasingly forgetful - ?dementia
Often takes his medication and forgets to eat
Family often find him in bed, drowsy, sweaty
Blood glucose on a glucometer during such
episodes 2-4mmol/l; responds to sugary drink
or food
Hba1c 32 mmol/l (5.1%)
Medication changed
Hypoglycaemia (‘Hypo’)
Symptoms (hypo awareness):
Feeling shaky, palpitations
Sweating
Hunger
Tiredness
Blurred vision
Lack of concentration
Headaches
Mood changes
Going pale.
Many people may lack warning symptoms
 
What causes a Hypo?
Excess insulin
Delayed or missed meal, not enough carbs
Unplanned physical activity,
Drinking large quantities of alcohol or alcohol
without food
Infections
 Sometimes there just is no obvious cause.
Treatment
If swallowing is intact and patient is conscious,
15–20g of fast-acting carbohydrate:
Small glass of sugary (non-diet) drink
At least three glucose tablets
Five sweets, such as jelly babies
Small carton of pure fruit juice
Glucose gel.
If unconscious:
Glucagon Injection
Call an ambulance: IV glucose
Diabetes & Driving
Group 1 driver (cars and motorbikes)
On insulin,  inform the DVLA (in the UK) or DVA (Northern Ireland).
Licence renewed every one, two, or three years.
Any changes which occur between renewals (e.g. complications which
might affect the ability to drive safely) should be reported when they
happen.
Drivers who are under medical supervision by a doctor do not need to
notify if insulin is used for a temporary period only
Group 1 driver on non-insulin medication for diabetes do not need to
notify unless:
Two episodes of severe hypoglycaemia within the last 12 months
Impaired awareness of hypoglycaemia
Disabling hypo whilst driving
Other medical conditions e.g.: problems with vision (e.g. laser
treatment/injections), circulation, or sensation (e.g. peripheral neuropathy).
Diabetes & Driving
Group 2 driver (bus or lorry)
Must inform the DVLA
Insulin treatment: independent medical assessment every year.
Should monitor blood glucose levels regularly and store results on a
memory meter.
Need to provide three months of continuous meter readings at
assessment.
Any changes to the condition or treatment should be reported
Safe driving:
On insulin, check blood glucose within two hours before getting
behind the wheel and every two hours whilst driving.
The DVLA advise that if blood glucose is 5mmol/l or less take
carbohydrate before driving. If it is less than 4mmol/l do not drive.
Diabetic driver jailed for impaling pedestrian
A driver who failed to tell the DVLA that he had diabetes has been jailed for six months and
banned from driving for three years leaving a pedestrian impaled on the railings after losing
control of his car when his blood-sugar level plummeted.
Diabetic Ketoacidosis (DKA)
Younger patient
May be the first presentation of T1D usually,
or in someone with pre-existing diabetes who
omits their insulin
Life threatening emergency
May occur with inter-current illness
Children: Puberty
Development of DKA
Acidosis
Dehydration
Hyperglycaemia
Insulin Resistance/
Deficiency
↑Lipolysis
↑FFA
↑Ketones
Vomiting
Hypotension 
& Shock
↓Cellular Glucose Uptake
Glycosuria
Osmotic Diuresis
What are ketones?
Ketones are produced
as a by product of fatty
acid synthesis in
response to starvation
3 types
Acetone
Acetoacetate
(acetoacetic acid)
β
 hydroxybutyrate (
β
hydroxybutyric acid)
Symptoms & Management
Increased thirst, polyuria
Weight loss
Abdominal pain, vomiting
Blurring of vision
Ketone breath
Tired, lethargic
Collapse
Treatment: monitored fluids and insulin, often
requires an intensive care setting
HHS/ Hyperosmolar Hyperglycaemic
State
Typically older patient
May be known to have T2 Diabetes or new
presentation
High mortality (15-20%)
Diagnosis (JBDS HHS Guidance 2012):
High osmolality >320 mosm/kg
High blood glucose30 mmol/L
Severely dehydrated and unwell
May be associated with impaired mental state
Associated infection, kidney disease, cardiovascular
disease
Management
The goals of treatment of HHS are to:
normalise the osmolality gradually and safely
replace fluid and electrolyte losses gradually and
safely
normalise blood glucose gradually and safely
treat the underlying cause
prevent arterial or venous thrombosis
prevent other potential complications e.g.
cerebral oedema/ central pontine myelosis
prevent of foot ulceration
Long Term or Chronic Complications
Diabetic Retinopathy:
Commonest cause of blindness in the working age
in UK
Three types:
Background retinopathy
Proliferative retinopathy
Maculopathy
Other eye disease: premature cataracts, glaucoma
Diabetic retinopathy
Proliferative retinopathy
Diabetic Maculopathy
Laser Photocoagulation
Diabetic Neuropathy
Damage to the small blood vessels supplying
the nerves
Three main types of neuropathy
:
Sensory
Motor
Autonomic
Sensory Neuropathy
Symptoms:
Tingling and numbness
Loss of ability to feel pain
Loss of ability to detect changes in
temperature
Loss of coordination due to loss of position
sense
Burning or shooting pains – these may be
worse at night time.
Sensory Neuropathy
Foot Ulcer
Charcot Joint
Motor Neuropathy
Symptoms:
Muscle weakness, which could cause falls or
problems with tasks such as fastening buttons.
Muscle wasting, where muscle tissue is lost
due to lack of activity
Muscle twitching and cramps.
Autonomic Neuropathy
Gastroparesis – when food can’t move through
the digestive system efficiently. Symptoms of this
can include bloating, constipation or diarrhoea
Loss of bladder control, leading to incontinence
Irregular heart beats
Problems with sweating, either a reduced ability
to sweat and intolerance to heat or sweating
related to eating food (gustatory)
Impotence (inability to keep an erection).
Cardiovascular Disease
Risk of developing & dying from CHD is 2-5
times higher with diabetes
Diabetes increases the risk of mortality or
serious morbidity  after a coronary event
1.5 to 3 fold
Smoking increases the risk of cardiovascular
death 4 fold in a person with diabetes
Patients of South Asian descent have 40%
higher risk of CHD
ABCDE…...
Secondary Prevention of CHD 
( 
Lancet 2001)
A
 
Aspirin
B
 
Beta Blockers
C
 
Cholesterol-lowering drugs
D
 
Diet; Diabetes; Don’t smoke
E
 
Exercise
Primary prevention:
Anti-hypertensive therapy: Aggressive lowering of
 
BP lowers cardiovascular morbidity & mortality; reduce
proteinuria
Tight blood glucose management
Lifestyle modification
Peripheral Vascular Disease
Loss of peripheral circulation
Intermittent Claudication
Foot Ulcer
Gangrene
Amputation
Cerebrovascular Disease
Common Manifestations:
TIA/Transient Ischaemic Attacks
Stroke
Cerebrovascular dementia
Managing people with Chronic Kidney
Disease
Reduce cardiovascular risk: lifestyle changes
Dietary advice: potassium, phosphate, calorie
and salt intake
Good blood sugar & BP management reduces
 
progression
Pharmacotherapy :
 
Sodium Bicarbonate –reduces metabolic
acidosis
 
Anti-platelet therapy to reduce CVD
 
Refer Renal Physicians
CKD - Management
Sodium Bicarbonate: Consider oral
supplementation to manage metabolic
acidosis
Vitamin D: may be used to treat CKD mineral
bone disorder
Anti-platelet therapy : Offer to prevent
secondary cardiovascular disease.
Risk & Progression
Risk factors
Cardiovascular disease
Proteinuria
Hypertension
Acute Kidney Injury
Diabetes
Smoking
African Caribbean, Asian origin
Long term use of NSAIDs
Untreated urinary outflow obstruction
The changing face of diabetic
pregnancy in UK
The Adult Obesity Time Bomb (One in 5 adults
in UK are now obese)
  
Type 2 diabetes epidemic
The Childhood Obesity Time Bomb
Multi-ethnicity in many health districts
Diabetes in pregnancy
Pre-existing T1 or T2 DM
Gestational Diabetes (GDM)
Risk factor for GDM include:
Obesity
Family history of diabetes
An unexplained stillbirth or neonatal death in a previous
pregnancy, and/or a very large infant in a previous pregnancy
(4.5kg / 10 pounds or over)
Previous gestational diabetes before
Family origin is South Asian, Black Caribbean or Middle
Eastern.
Major problems arising from
diabetes in pregnancy
Increased risk of stillbirth, neonatal death
Increased risk of major congenital malformations
(
pre-existing diabetes
)
 
 
2 to 5 fold increase in risk
Macrosomia (all types) 
 shoulder dystocia etc
Neonatal hypoglycaemia (all types)
Major congenital malformations associated with
maternal diabetes
Cardiac:
Transposition of great vessels,
ventricular septal defect,
situs inversus,
single ventricle,
hypoplastic left ventricle
CNS:
 
Anencephaly, encephalocoele, meningomyelocele, Spina Bifida
Renal:
Agenesis, multicystic dysplasia
Pulmonary:
Hypoplasia
Gastrointestinal:
Anal/rectal atresia, small left colon
Confidential Enquiry into Maternal and Child
Health (CEMACH); Diabetes Study
Study of pregnancy in women with pre-existing diabetes 2002/03
Prevalence of type 2 diabetes linked to ethnicity and socio-
economic status
Stillbirth rate 26.8 per 1000 v 5.7
Perinatal Mortality Rate 31.8 per 1000 v 8.5
Major congenital abnormalities increased by x 2
No difference between Type 1 and Type 2 diabetes
Screening for foetal malformations
In women with pre-existing diabetes:
Detailed fetal ultrasound at 18 to 20 weeks to
exclude congenital anomalies
foetal cardiac anomaly scan
Pre-pregnancy preparation
in type 2 diabetes
Should include:
Optimise Blood Glucose control (and remain on reliable contraception in
interim)
Start Folic Acid 5 mg od
Stop lipid lowering drug therapy
Change anti-hypertensive therapy to Methyl Dopa or Labetolol
Review status of microvascular disease
The Diabetes Annual Review
Examination
 
Examine:
Feet
Peripheral Pulses
Peripheral Nerves
BP
Eyes
Blood tests:
Hba1c – blood glucose
Renal Function
Lipid Screen
Urine Protein
THANK YOU
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"Explore acute and short-term complications of diabetes, including hypoglycemia and hyperglycemia. Learn about real-life cases and their management strategies. Discover the symptoms of hypoglycemia, common causes, and effective treatments to address this serious condition. Understand the importance of timely intervention and proper care in diabetic emergencies."

  • Diabetes
  • Complications
  • Hypoglycemia
  • Hyperglycemia
  • Treatment

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  1. Complications of Diabetes Dr Shanti Vijayaraghavan, Consultant Diabetologist, Barts Health, London 15 May 2015

  2. Acute or Short-term Complications 1. Hypoglycaemia: low blood glucose level 2. Hyperglycaemia: Diabetic Ketoacidosis (DKA) Hyperosmolar Hyperglycaemic State (HHS)

  3. CB, 32/F Primary school teacher, type 1 DM of 14 years duration (autoimmune) September 2014: Change of job - desk-based to more active job Started cycling to work Sensible diet and plenty of exercise BMI 23, on Novorapid insulin with each meal, and glargine insulin at night January 2015: Very erratic blood glucose control with frequent hypoglycaemia during the day (upto 10/day) No hypoglycaemia awareness March 2015: In a school meeting pre-lunch Sudden loss of conciousness with ? Seizure Taken to local A & E Blood glucose 1.5 mmol/l requiring IV glucose drips

  4. AC, 82 M Type 2 diabetes for 30 years Son reports increasingly forgetful - ?dementia Often takes his medication and forgets to eat Family often find him in bed, drowsy, sweaty Blood glucose on a glucometer during such episodes 2-4mmol/l; responds to sugary drink or food Hba1c 32 mmol/l (5.1%) Medication changed

  5. Hypoglycaemia (Hypo) Symptoms (hypo awareness): Feeling shaky, palpitations Sweating Hunger Tiredness Blurred vision Lack of concentration Headaches Mood changes Going pale. Many people may lack warning symptoms

  6. What causes a Hypo? Excess insulin Delayed or missed meal, not enough carbs Unplanned physical activity, Drinking large quantities of alcohol or alcohol without food Infections Sometimes there just is no obvious cause.

  7. Treatment If swallowing is intact and patient is conscious, 15 20g of fast-acting carbohydrate: Small glass of sugary (non-diet) drink At least three glucose tablets Five sweets, such as jelly babies Small carton of pure fruit juice Glucose gel. If unconscious: Glucagon Injection Call an ambulance: IV glucose

  8. Diabetes & Driving Group 1 driver (cars and motorbikes) On insulin, inform the DVLA (in the UK) or DVA (Northern Ireland). Licence renewed every one, two, or three years. Any changes which occur between renewals (e.g. complications which might affect the ability to drive safely) should be reported when they happen. Drivers who are under medical supervision by a doctor do not need to notify if insulin is used for a temporary period only Group 1 driver on non-insulin medication for diabetes do not need to notify unless: Two episodes of severe hypoglycaemia within the last 12 months Impaired awareness of hypoglycaemia Disabling hypo whilst driving Other medical conditions e.g.: problems with vision (e.g. laser treatment/injections), circulation, or sensation (e.g. peripheral neuropathy).

  9. Diabetes & Driving Group 2 driver (bus or lorry) Must inform the DVLA Insulin treatment: independent medical assessment every year. Should monitor blood glucose levels regularly and store results on a memory meter. Need to provide three months of continuous meter readings at assessment. Any changes to the condition or treatment should be reported Safe driving: On insulin, check blood glucose within two hours before getting behind the wheel and every two hours whilst driving. The DVLA advise that if blood glucose is 5mmol/l or less take carbohydrate before driving. If it is less than 4mmol/l do not drive. Diabetic driver jailed for impaling pedestrian A driver who failed to tell the DVLA that he had diabetes has been jailed for six months and banned from driving for three years leaving a pedestrian impaled on the railings after losing control of his car when his blood-sugar level plummeted.

  10. Diabetic Ketoacidosis (DKA) Younger patient May be the first presentation of T1D usually, or in someone with pre-existing diabetes who omits their insulin Life threatening emergency May occur with inter-current illness Children: Puberty

  11. Development of DKA Acidosis Ketones FFA Vomiting Lipolysis Catecholamines Cortisol Growth Hormone AVP Hypotension & Shock Dehydration Insulin Resistance/ Deficiency Osmotic Diuresis Cellular Glucose Uptake Glycosuria Hyperglycaemia

  12. What are ketones? Ketones are produced as a by product of fatty acid synthesis in response to starvation 3 types Acetone Acetoacetate (acetoacetic acid) hydroxybutyrate ( hydroxybutyric acid)

  13. Symptoms & Management Increased thirst, polyuria Weight loss Abdominal pain, vomiting Blurring of vision Ketone breath Tired, lethargic Collapse Treatment: monitored fluids and insulin, often requires an intensive care setting

  14. HHS/ Hyperosmolar Hyperglycaemic State Typically older patient May be known to have T2 Diabetes or new presentation High mortality (15-20%) Diagnosis (JBDS HHS Guidance 2012): High osmolality >320 mosm/kg High blood glucose30 mmol/L Severely dehydrated and unwell May be associated with impaired mental state Associated infection, kidney disease, cardiovascular disease

  15. Management The goals of treatment of HHS are to: normalise the osmolality gradually and safely replace fluid and electrolyte losses gradually and safely normalise blood glucose gradually and safely treat the underlying cause prevent arterial or venous thrombosis prevent other potential complications e.g. cerebral oedema/ central pontine myelosis prevent of foot ulceration

  16. Long Term or Chronic Complications Diabetic Retinopathy: Commonest cause of blindness in the working age in UK Three types: Background retinopathy Proliferative retinopathy Maculopathy Other eye disease: premature cataracts, glaucoma

  17. Diabetic retinopathy

  18. Proliferative retinopathy

  19. Diabetic Maculopathy

  20. Laser Photocoagulation

  21. Diabetic Neuropathy Damage to the small blood vessels supplying the nerves Three main types of neuropathy: Sensory Motor Autonomic

  22. Sensory Neuropathy Symptoms: Tingling and numbness Loss of ability to feel pain Loss of ability to detect changes in temperature Loss of coordination due to loss of position sense Burning or shooting pains these may be worse at night time.

  23. Sensory Neuropathy Foot Ulcer Charcot Joint

  24. Motor Neuropathy Symptoms: Muscle weakness, which could cause falls or problems with tasks such as fastening buttons. Muscle wasting, where muscle tissue is lost due to lack of activity Muscle twitching and cramps.

  25. Autonomic Neuropathy Gastroparesis when food can t move through the digestive system efficiently. Symptoms of this can include bloating, constipation or diarrhoea Loss of bladder control, leading to incontinence Irregular heart beats Problems with sweating, either a reduced ability to sweat and intolerance to heat or sweating related to eating food (gustatory) Impotence (inability to keep an erection).

  26. Cardiovascular Disease Risk of developing & dying from CHD is 2-5 times higher with diabetes Diabetes increases the risk of mortality or serious morbidity after a coronary event 1.5 to 3 fold Smoking increases the risk of cardiovascular death 4 fold in a person with diabetes Patients of South Asian descent have 40% higher risk of CHD

  27. ABCDE... Secondary Prevention of CHD ( Lancet 2001) A Aspirin B Beta Blockers C Cholesterol-lowering drugs D Diet; Diabetes; Don t smoke E Exercise Primary prevention: Anti-hypertensive therapy: Aggressive lowering of BP lowers cardiovascular morbidity & mortality; reduce proteinuria Tight blood glucose management Lifestyle modification

  28. Peripheral Vascular Disease Loss of peripheral circulation Intermittent Claudication Foot Ulcer Gangrene Amputation

  29. Cerebrovascular Disease Common Manifestations: TIA/Transient Ischaemic Attacks Stroke Cerebrovascular dementia

  30. Managing people with Chronic Kidney Disease Reduce cardiovascular risk: lifestyle changes Dietary advice: potassium, phosphate, calorie and salt intake Good blood sugar & BP management reduces progression Pharmacotherapy : Sodium Bicarbonate reduces metabolic acidosis Anti-platelet therapy to reduce CVD Refer Renal Physicians

  31. CKD - Management Sodium Bicarbonate: Consider oral supplementation to manage metabolic acidosis Vitamin D: may be used to treat CKD mineral bone disorder Anti-platelet therapy : Offer to prevent secondary cardiovascular disease.

  32. Risk & Progression Risk factors Cardiovascular disease Proteinuria Hypertension Acute Kidney Injury Diabetes Smoking African Caribbean, Asian origin Long term use of NSAIDs Untreated urinary outflow obstruction

  33. The changing face of diabetic pregnancy in UK The Adult Obesity Time Bomb (One in 5 adults in UK are now obese) Type 2 diabetes epidemic The Childhood Obesity Time Bomb Multi-ethnicity in many health districts

  34. Diabetes in pregnancy Pre-existing T1 or T2 DM Gestational Diabetes (GDM) Risk factor for GDM include: Obesity Family history of diabetes An unexplained stillbirth or neonatal death in a previous pregnancy, and/or a very large infant in a previous pregnancy (4.5kg / 10 pounds or over) Previous gestational diabetes before Family origin is South Asian, Black Caribbean or Middle Eastern.

  35. Major problems arising from diabetes in pregnancy Increased risk of stillbirth, neonatal death Increased risk of major congenital malformations (pre-existing diabetes) 2 to 5 fold increase in risk Macrosomia (all types) shoulder dystocia etc Neonatal hypoglycaemia (all types)

  36. Major congenital malformations associated with maternal diabetes Cardiac: Transposition of great vessels, ventricular septal defect, situs inversus, single ventricle, hypoplastic left ventricle CNS: Anencephaly, encephalocoele, meningomyelocele, Spina Bifida Renal: Agenesis, multicystic dysplasia Pulmonary: Hypoplasia Gastrointestinal: Anal/rectal atresia, small left colon

  37. Confidential Enquiry into Maternal and Child Health (CEMACH); Diabetes Study Study of pregnancy in women with pre-existing diabetes 2002/03 Prevalence of type 2 diabetes linked to ethnicity and socio- economic status Stillbirth rate 26.8 per 1000 v 5.7 Perinatal Mortality Rate 31.8 per 1000 v 8.5 Major congenital abnormalities increased by x 2 No difference between Type 1 and Type 2 diabetes

  38. Screening for foetal malformations In women with pre-existing diabetes: Detailed fetal ultrasound at 18 to 20 weeks to exclude congenital anomalies foetal cardiac anomaly scan

  39. Pre-pregnancy preparation in type 2 diabetes Should include: Optimise Blood Glucose control (and remain on reliable contraception in interim) Start Folic Acid 5 mg od Stop lipid lowering drug therapy Change anti-hypertensive therapy to Methyl Dopa or Labetolol Review status of microvascular disease

  40. The Diabetes Annual Review Examination Examine: Feet Peripheral Pulses Peripheral Nerves BP Eyes Blood tests: Hba1c blood glucose Renal Function Lipid Screen Urine Protein

  41. THANK YOU

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