17. Acute complications of diabetes Flashcards
What are some acute complications of diabetes?
Diabetic ketoacidosis • Absolute insulin deficiency Hyperosmolar hyperglycaemia sate • Relative insulin deficiency Hypoglycaemia Relative insulin excess
Pathophysiology of DKA
Unchecked gluconeogenesis -> Hyperglycaemia
Osmotic diuresis ->
Dehydration
Unchecked ketogenesis -> Ketosis
Dissociation of ketone bodies into hydrogen ion and anions -> Anion-gap metabolic acidosis
Often a precipitating event is identified (infection, lack of insulin administration)
adipose tissue - physiological effects of insulin deficiency
Increased lipolysis and reduced esterification of fat
Insulin deficiency
Glucagon/adrenaline excess
Results in excess FFA and glycerol from breakdown triglycerides
FFA substrate for hepatic synthesis of ketone bodies
Acetoacetate/Hydroxybutyrate – strong organic acids
(Acetone)
Rate of ketogenesis is linked to rate of gluconeogenesis
Muscle and brain can utilise ketones as main energy substrate
Ketoacidosis results when ketone body production exceeds rate of utilisation in peripheral tissues (brain and muscle) and renal clearance
DKA metabolic derangement
Acidosis managed by Intracellular buffering - H+ / K+ exchange Potassium hydrogen ion pump Respiratory compensation – hyperventilation H+ stimulates respiratory centres Breathe off CO2 (H+ + HCO3- H2O + CO2) Renal excretion of H+ (slow response) Electrolyte disturbances – renal losses Potassium depletion – maybe >250mmol Sodium depletion - dehydration
Diabetic ketoacidosis clinical features
Age Mostly young T1DM Precipitating causes Relative or absolute insulin deficiency Serum sodium Normal or low Blood glucose Usually <40mmol/l Serum bicarbonate/pH <14mmol/l / pH<7.3 Serum ketones +++++ Mortality 5% depending on age Subsequent course Insulin dependent
DKA precipitating factors
Infections – pneumonia, urinary tract, viral illnesses, gastroenteritis Error/ missed insulin administration Myocardial infarction Previously undiagnosed Type 1 diabetes Drugs: steroids Unidentified
DKA symptoms and signs caused by hyperglycaemia and dehydration
Symptoms:
Thirst and polyuria
Weakness and malaise
Drowsiness, confusion
Signs:
Dry mouth, Sunken eyes
Postural or supine hypotension
Hypothermia & Coma
DKA signs and symptoms caused by acidosis
Symptoms: Nausea and vomiting
Abdominal pain
Breathlessness
Signs: Facial flush
Hyperventilation
Smell of ketones on breath and ketonuria
DKA management
correct the metabolic derangement
5 Step Plan:
Confirm diagnosis and check for precipitating causes
Rehydrate & 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
Other DKA management factors
Is the patient conscious? Assess GCS If concern, call ITU 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 >40years
Precipitating causes:
previously undiagnosed, steroids, diuretics, sugar
Serum sodium:
Usually high
Blood glucose:
Often >40mmol/l
Serum bicarbonate/pH:
Normal / pH 7.4
Serum ketones: 0
Mortality: 30% (thromboses)
Subsequent course:
Diet/tablet controlled
HHS management
Correct the profound dehydration
Confirm diagnosis and check for precipitating causes
Rehydrate & monitor fluid balance
Iv fluids - saline with added potassium
Consider urinary catheter
Lower glucose (once glucose not improving with fluids)
Intravenous 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.
What is hypoglycaemia?
Hypoglycaemia is a biochemical term and exists when blood sugar < 4mmol/l but is often used to describe a clinical state. The clinical syndrome associated with hypoglycaemia develops as the nervous system becomes glucose deficient or ‘neuroglycopaenic’. It can be classified:
Asymptomatic
Awake
sleeping
Mild symptomatic (patient can treat himself)
Severe symptomatic (help needed by third party)
Coma and convulsions
hypoglycaemia symptoms
Autonomic – sympathomedullary activation Sweating, feeling hot Trembling or shakiness Anxiety palpitations
Neuroglycopenic Dizziness, light-headedness Tiredness Hunger, nausea Headache Inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural change, automatism Coma and convulsions, hemiplegia
hypoglycaemia causes
Insulin
Inappropriately excessive doses
Not eating, or insufficient carbohydrate
Sulfonylureas
hypoglycaemia counter-regulation
Glucagon, adrenaline, cortisol and GH all have ‘anti-insulin effects’
Glucagon stimulates glycogenolysis and gluconeogenesis and is probably primary response
Adrenaline increases glycogenolysis
GH and cortisol limit glucose disposal in peripheral tissues, but this effect takes several hours so of little benefit acutely
Sympathetic nerves may also directly activate hepatic glycogenolysis and stimulate glucagon secretion
Hypoglycaemia treatment
Minor episodes
20g carbohydrate as sugary drink, fruit juice, glucose tablets, glucose gels followed by something ‘starchy’ to eat
Glucose gels
Hypoglycaemic coma
im or iv Glucagon 1mg
iv dextrose 25g (150ml 10% glucose)
Mild/moderate hypo
Patient conscious, orientated and able to swallow.
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Give 5 level teaspoons glucose powder in water or 120mls Lucozade or 5 glucose tablets Test blood glucose after 15 minutes. If < 4 mmol/l repeat up to 3 times
If this has been repeated 3 times, consider 10% glucose IV 100 ml/hr or 1 mg Glucagon IM
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Give long acting carbohydrate e.g. 2 biscuits or a slice of bread or next meal if due.
DO NOT OMIT SUBSEQUENT DOSES OF INSULIN
GLUCAGON CAN ONLY BE GIVEN ONCE DAILY. IT WILL NOT REVERSE HYPOGLYCAEMIA IN PATIENTS WITH RECURRENT HYPOS, ANOREXIA OR SEVERE LIVER DISEASE
severe hypoglycaemia treatment
Patient unconscious / fitting / very aggressive or nil by mouth (NBM)
->
Check ABC, Stop any IV insulin
If patient suitable for IM Glucagon give 1 mg . If not give 10% IV glucose 150ml. Repeat up to 3 times
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Recheck glucose level after 15 minutes it should now be above 4mmol/L. Give long acting carbohydrate e.g. 2 biscuits or a slice of bread or next meal if due. If NBM give 10% glucose infusion at 100ml/hr until no longer NBM
DKA overview
DKA
Insulin deficiency > ketosis > acidosis
Treat with insulin, fluids and potassium
HSS
HSS
Old, frail, often precipitating factor
Relative insulin deficiency > hyperglycaemia > profound dehydration
Treat with fluids… insulin
Hypo
Hypo
Too much insulin
Treat with glucose
