Acute complications of diabetes Flashcards
Diabetic ketoacidosis: pathophysiology
Unchecked gluconeogenesis –> hyperglycaemia
Osmotic diuresis –> dehydration
Unchecked ketogenesis –> ketosis
Dissociation of ketone bodies into H+ and anions –> anion gap metabolic acidosis
Adipose tissue- physiological effects of insulin deficiency
Increased lipolysis and reduced esterification of fat
FFA substrate for hepatic synthesis of ketone bodies
Muscle and brain can utilise ketones as main energy substrate
Ketoacidosis results when ketone body production exceeds rate of utilisation in peripheral tissues and renal clearance
DKA- acidosis managed by
Intracellular buffereing - H+/K+ exchange
Respiratory compensation - hyperventilation
- H+ stimulates respiratory centres
- breathe off CO2
Renal excretion of H+ (slow response)
DKA- electrolyte disturbances (renal losses)
Potassium depletion
Sodium depletion
Dehydration
Extracellular [K]
4mmol/l
Intracellular [K]
125mol/l
DKA precipitating factors
Infections- pneumonia, urinary tract, viral illnesses, gastroenteritis
Error/ missed insulin administration
MI
Previously undiagnosed type 1 diabetes
Drugs: steroids
Symptoms of DKA
Thirst and polyuria
Weakness and malaise
Drowsiness, confusion
Nausea and vomiting
Abdominal pain
Breathlessness
Signs and symptoms of hyperglycaemia and dehydration
Symptoms
- thirst and polyuria
- weakness and malaise
- drowsiness, confusion
Signs
- dry mouth
- sunken eyes
- postural or supine hypotension
- hypothermia and coma
Signs and symptoms of acidosis
Symptoms
- nausea and vomiting
- abdominal pain
- breathlessness
Signs
- facial flush
- hyperventilation
- smell of ketones on breath and ketonuria
Clinical features of DKA
Age: mostly young T1DM
Cause: relative or absolute insulin deficiency
Serum sodium: normal or low
Blood glucose: usually <40mml/l
Serum HCO3-/pH: <14mmol/l / ph<7.3
Serum ketones: high
Mortality: 5% depending on age
DKA 5 step plan
- Confirm diagnosis and check for precipitating causes
- Rehydrate and monitor fluid balance
- IV fluids- saline with added potassium
- consider urinary catheter - Lower glucose
- intravenous insulin- fixed rate 0.1unit/kg/hr - Monitor electrolytes
- potassium (and sodium) - Prevent clots
- prophylactic low molecular weight heparin
DKA other management factors
Is the patient conscious?
- assess GCS
At risk of aspiration
- consider NG tube
Monitor recovery
- glucose, ketones, pH, potassium hourly
DKA recovery
pH normal, ketones <2+ (urine), vomiting settled
Resume normal diet
Switch from intravenous to normal subcutaneous insulin
Hyperosmolar hyperglycaemic state clinical features
Age: usually .40
Precipitating causes: previously undiagnosed, steroids, diuretics, sugar
Serum sodium: usually high
Blood glucose: often >40mmol/l
Serum HCO3/ pH: normal/ pH 7.4
Serum ketones: 0
Mortality: 30%
HHS management
Confirm diagnosis and check for precipitating causes
Rehydrate and monitor fluid balance
- IV fluids- saline with added potassium
- consider urinary catheter
Lower glucose (once glucose not improving with fluids) - IV insulin fixed rate 0.05unit/kg/hr
Monitor electrolytes
- potassium (and sodium)
Prevent clots
- treatment low molecular weight heparin
Patients are often elderly and severely ill
Hypoglycaemia
Blood sugar <4mmol/l
Asymptotic
- awake
- sleeping
Mild symptomatic (patient can treat themselves)
Severe symptomatic (help needed)
Coma and convulsions
Autonomic symptoms of hypoglycaemia
Sweating, feeling hot
Trembling or skakiness
Anxiety
Palpitations
Neuroglycopenic symptoms of hypoglycaemia
Dizziness, light headedness
Tiredness
Hunger, nausea
Headache
Inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural changes, automatism
Coma and convulsions, hemiplegia
Causes of hypoglycaemia
Insulin
- inappropriately excessive doses
- not eating, or insufficient carbohydrate
Sulfonylureas
Hyperglycaemia- counter regulations
Glucagon, adrenaline, cortisol and GH all have anti insulin effect
Glucagon stimualtes glycogenolysis and gluconeogenesis (1)
Adrenaline increases glycogenolysis
GH and cortisol limit glucose disposal in peripheral tissues, takes several hours
Sympathetic nerves may directly activate hepatic glycogenolysis and stimulate glucagon secretion
Treatment of minor episode of hypoglycaemia
20mg carbohydrate as sugary drink, fruit juice, glucose tablets, glucose gels followef by something starchy to eat
Glucose gels
Treatment of hypoglycaemic coma
IM or IV glucagon 1mg
IV dextrose 25mg (150ml 10% glucose)
