L17 - Diabetic Emergencies Flashcards
Pathophysiology of diabetic ketoacidosis
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)
How does insulin deficiency lead to CV collapse?
Insulin deficiency => hyperglycaemia => hyperosmolality and glycosuria => dehydration and electrolyte losses
Dehydration => renal failure => shock
shock => CV COLLAPSE
Insulin deficiency => CV collapse via LIPOLYSIS
Insulin deficiency => lipolysis => increased FFAs => ketones => acidosis => CV collapse
What is the connection between to two routes to CV collapse as a result of insulin deficiency?
Hyperglycaemia leads to glycosuria which leads to electrolyte losses
AND ALSO
lipolysis leads to acidosis which leads to electrolyte losses
BOTH these routes lead to CV collapse
Clinical features of diabetic ketoacidosis: age
mostly young T1DM
Clinical features of diabetic ketoacidosis: precipitating causes
relative or absolute insulin deficiency
Diabetic ketoacidosis - precipitating factors
Infections - pneumonia, urinary tract, viral illnesses, gastroenteritis
Error/missed insulin administration
MI
Previously undiagnosed T1DM
Drugs: steroids
Unidentified
Diabetic ketoacidosis - symptoms and signs
Symptoms of thirst and polyuria, weakness and malaise, drowsiness, confusion caused by hyperglycaemia + dehydration
Signs of these are dry mouth, sunken eyes, postural or supine hypotension, hyperthermia and coma
Other symptoms of nausea and vomiting, abdominal pain and breathlessness are caused by acidosis
Signs of these are facial flush, hyperventilation, smell of ketones on breath and ketonuria
Clinical features of diabetic ketoacidosis: serum sodium
normal or low
Clinical features of diabetic ketoacidosis: blood glucose
usually <40mmol/l
Clinical features of diabetic ketoacidosis: serum bicarbonate/pH
<14mmol/l / pH<7.3
Clinical features of diabetic ketoacidosis: serum ketones
+++++
Clinical features of diabetic ketoacidosis: mortality
5% depending on age
Clinical features of diabetic ketoacidosis: subsequent course
insulin dependent
Diabetic ketoacidosis - Management
5 step plan
1) Confirm diagnosis and check for precipitating causes
2) Rehydrate & monitor fluid balance
- IV fluids - saline with added potassium
- Consider urinary catheter
3) Lower glucose
- IV insulin - fixed rate 0.1Unit/kg/hr
4) Monitor electrolytes
- Potassium (and sodium)
5) Prevent clots
- Prophylactic low molecular weight heparin
Diabetic ketoacidosis - other 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
Diabetic ketoacidosis - recovery
pH normal, ketones <2+ (urine), vomiting settled
- resume normal diet
- switch from IV to normal subcutaneous insulin
HHS stands for
hyperosmolar hyperglycaemic state
Pathway of HHS
Insulin deficiency and glucagon adrenaline (cortisol) both cause glycogenolysis
Glycogenolysis along with increased intake of sugary drinks leads to increased hepatic glucose output and hyperglycaemia
This leads to osmotic diuresis
=> DEHYDRATION
Hyperosmolar Hyperglycaemic State – clinical features: age
Usually >40years
Hyperosmolar Hyperglycaemic State – clinical features: precipitating causes
Previously undiagnosed, steroids, diuretics, sugar
Hyperosmolar Hyperglycaemic State – clinical features: serum sodium
Usually high
Hyperosmolar Hyperglycaemic State – clinical features: serum bicarbonate/pH
Normal/ pH 7.4
Hyperosmolar Hyperglycaemic State – clinical features: serum ketones
0
Hyperosmolar Hyperglycaemic State – clinical features: mortality
30% (thromboses)
Hyperosmolar Hyperglycaemic State – clinical features: subsequent course
Diet/tablet controlled
HHS - Management
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) -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
Causes of hypoglycaemia
Too little food or skip a meal; too much insulin or diabetes pills; more active than usual
Onset of hypoglycaemia
Often sudden; may pass out if untreated
Definition of hypoglycaemia
Hypoglycaemia is a biochemical term and exists when blood sugar < 4mmol/l but often used to describe a clinical state.
The clinical syndrome associated with hypoglycaemia develops as the nervous system becomes glucose deficient or ‘neuroglycopaenic’.
Hypoglycaemia can be classified as:
asymptomatic
- awake
- sleeping
mild symptomatic (patient can treat himself)
severe symptomatic (help needed by their party)
coma and convulsions
Autonomic symptoms of hypoglycaemia
Autonomic - sympathomedullary activation
sweating, feeling hot
trembling or shakiness
anxiety
palpitations
Neuroglycopenic symptoms of hypoglycaemia
dizziness, light-headedness
tiredness
hunger, nausea
headache
inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural change, automatism
coma and convulsions, hemiplegia
Causes of hypoglycaemia
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)
