One of the biggest problems is that there are several complications associated with these conditions:
- Non-enzymatic glycosylation (NEG) of macrovessels – this leads to atherosclerosis
– Causes cardiovascular disease – MI is 4x more common in diabetes and stroke 2x common
– Causes peripheral vascular disease – leading cause of non-traumatic amputations.
– If foot pulses cannot be felt, use Doppler pressure measurements. Ensure regular chiropody to remove callus to reduce risk of ulcers
- Non-enzymatic glycosylation (NEG) of microvessels – leads to hyaline arteriosclerosis
– Causes Nephropathy – nephrotic syndrome characterized by Kimmelstiel-Wilson nodules in glomeruli
– Gives microalbuminuria (when the urine dipstick is negative for protein but the urine albumin:creatinine ratio is >4mg/mmol)
– Diabetic patients get annual screening to measuring morning albumin:creatinine ratio
- Diabetic retinopathy – glucose enters Schwan cells, the lens and retinal blood vessels damaging them
– Results in osmotic damage
– Leads to Cataracts + Rubeosis iridis (new vessels on iris leading to glaucoma)
– Diabetes is the leading cause of blindness in the developed world.
- Diabetic peripheral neuropathy – This is loss of sensation which often occurs in the feet
– Patient shows loss of sensation in “stocking” distribution + numbness/tingling
– Also leads to neuropathic deformity e.g. claw toes, Charcot Joint
– Pain is felt, worse at night –> 1st line treatment is Duloxetine
- Diabetic Autonomic Neuropathy
– Causes decreased lower oesophageal sphincter pressure giving GORD
– Can lead to chronic diarrhoae worse at night
– Gastroparesis –> Bloating and vomiting, alleviated with prokinetic antimimetics
- Hyperosmolar Hyperglycaemic State – This is where hyperglycaemia results in osmotic diuresis, severe dehydration and electrolyte deficiencies.
– High glucose leads to osmotic diuresis with loss of sodium and potassium
– Gives severe volume depletion giving raised serum osmolality (>320mosmol/kg), making blood viscous
General malaise –> Fatigue, nausea + vomiting
Neurological –> Low consciousness, headaches, papilloedema
Haematological –> MI and peripheral thrombosis (due to hyperviscosity)
Cardiovascular –> Tachycardia + Hypotension (similar to hypovolaemic shock)
- Marked Hyperglycaemia (>30 mmol/L) without much ketones or acidosis
- Significantly raised serum osmolarity (> 320 mosmol/kg)
Management – manage in HDU.
– 1st fluid resuscitation – IV 0.9% sodium chloride solution
– 2nd normalise blood glucose – only give insulin if ketones are high, as fluids will naturally reduce glucose
– If no ketones avoid insulin, as it leads to a rapid decline in glucose and serum osmolality increasing risk of central pontine myelinosis or cardiovascular collapse
– 3rd replace potassium as required – prevents arrhythmias.
This is the most common endocrine emergency characterized by plasma glucose <3mM.
Causes: Diabetic – Insulin or sulphonylurea treatment e.g. increased activity missed meal, overdose.
Non-Diabetic – The causes of non-diabetic hypoglycaemia are remembered by acronym (EXPLAIN).
The cause can be found by taking drug history , excluding liver failure and monitoring.
EX = Exogenous drugs
Symptoms – Autonomic – sweating, anxiety, tremor, dizziness
Neurological – Confusion, drowsiness, can be confused with a stroke
Treatment – If conscious, 15-20g of fast carbohydrate snack (orange juice) and recheck glucose after 10 min
– If conscious but not cooperative –> put glucose gel between teeth and gums
– If unconscious –> start glucose IV (10% and 200mL/15min) or glucagon 1mg IM (not in malnourished)
– Once blood glucose >4mM, give long acting carbohydrate e.g. slice of toast.
This is a benign pancreatic islet cell tumour which is sporadic or commonly seen with MEN-1
Symptoms – fasting hypoglycaemia with mental status change that is relieved by administration of glucose
Whipple’s triad –> Symptoms associated with fasting/exercise
–> Recording hypoglycaemia with symptoms
–> Symptoms relieved by glucose
Diagnosis – Give insulin and measure C-peptide levels
– This is because exogenous insulin usually inhibits C-peptide production, but not in an insulinoma
– You will therefore find low serum glucose levels in the presence of high insulin and C-peptide
Treatment – Surgical excision
3. J. Terrence Jose Jerome / CC BY (https://creativecommons.org/licenses/by/3.0)