Diabetic Emergencies Flashcards
Who is effected by Diabetic ketoacidosis?
Type 1 diabetics
Describe the pathophysiology of Diabetic ketoacidosis
Caused by hyperglycaemia causing Hyperglycaemia resulting in osmotic diuresis and electrolyte abnormalities.
Lack of insulin = glucose accumulates in blood
Glucose is not being used, body thinks it needs more energy. Increases in glycogenolysis and gluconeogenesis
]This is coupled with an increase in counter-regulatory hormone release (e.g. cortisol, glucagon, growth hormone), which exacerbates the hyperglycaemia and drives the production of alternative energy sources.
The lack of utility of glucose leads to the break down of fats (lipolysis) that increases serum free fatty acids. Fatty acids can be used as an alternative energy source through ketogenesis.
This increases the levels of ketone bodies
What is the biochemical abnormality triad which characterises Diabetic ketoacidosis
Hyperglycaemia: > 14.0 mmol/L or known DM
Ketonaemia: ≥ 3 mmol/L or significant ketonuria (> 2+ on dipstick)
Acidosis: bicarbonate < 15.0 mmol/L and/or venous pH < 7.3
What are the main ketone bodys within DKA?
3-beta-hydroxybutyrate
acetoacetic acid
List 5 main precipitants of DKA
Infection: 30-40% Non-compliance: 25% Inappropriate dose alteration: 13% New diagnosis of diabetes: 10-20% Intoxication / drugs Myocardial infarction: 1%
What are the signs and symptoms of DKA?
Symptoms
- Polyuria
- Polydipsia
- Nausea
- Vomiting
- Abdominal pain
- Leg cramps
- Headache
Signs
- Kussmaul breathing
- Ketotic breath
- Dehydration
- Hypotension
- Abdominal tenderness
- Reduced consciousness
- Coma
How is DKA diagnosed?
based on identification of the biochemical triad of hyperglycaemia, acidaemia and ketonaemia/ketonuria.
Laboratory glucose: > 14.0 mmol/L
Venous/arterial blood gas: pH < 7.3 or bicarbonate < 15 mmol/L
Ketone testing: capillary blood ketone ≥ 3 mmol/L or urinary ketones +++ or above
Frequently raised Urea and Creatinine
Which type 2 diabetic patients are at risk of DKA?
Some patients with T2DM are at risk of diabetic ketoacidosis. These patients are referred to as ketosis-prone. African Caribbean patients are particularly at risk.
What is Euglycaemic DKA?
DKA with normal or near-normal blood glucose levels
may occur in the presence of exhausted glycogen stores in the liver (e.g. protracted vomiting, alcohol use, malnutrition).
Which drug is known to cause Euglycaemic DKA?
sodium-glucose co-transporter-2 inhibitors (SGLT-2 inhibitors).
How is DKA treated?
ABCDE assessment
Investigations-
Intravenous access (x2 large bore cannula)
Blood / urinary ketones
Capillary & plasma blood glucose
HbAIc
FBC, U&Es, venous blood gas (VBG)
Blood cultures
Urinalysis +/- MSU,
Pregnancy test (as indicated) ECG
Cardiac monitoring
Establish usual diabetic pharmacotherapy
- Fluid assessment (catheter)
- 0.9% normal saline
- Especially in hypotension- Systolic BP < 90 mmHg
- If BP does not improve seek help
- Potassium replacement
- fixed rate intravenous short acting insulin- actropid infusion (FRIII) immediately, which is based on the patients weight - 0.1 units/kg/hr
If the patient is usually on a long-acting insulin therapy then this should be continued during the fixed rate intravenous insulin infusion
How are patients being treated with DKA monitored?
Patients should be monitored regularly to assess for an adequate fall in ketones, glucose and rise in bicarbonate with normalisation of acid-base balance.
Each hour, blood ketones and blood glucose should be checked.
A venous blood gas should be used for the pH and bicarbonate at 1 hour and 2 hours, and then 2 hours thereafter.
Potassium should be checked as a minimum of every 4 hours within the first 24 hours, but sooner if abnormal.
In those with severe DKA, they should have continual cardiac and saturation monitoring.
accurate fluid balance should be kept. Use catheter if required
Level 2 bed (High Dependency Unit)
Cardiac monitor
Nasogastric tube if impaired conscious level
Consider Central Venous Pressure line – especially in elderly
Oxygen if PaO2 < 10.5 kPa on air
Urinary catheter
Prophylactic LMW heparin
iv antibiotics as appropriate if suspected infection
Frequent monitoring of conscious level, BP, Pulse, Temp, Glucose, Urine
output, Potassium, Acidosis
What are the Metabolic treatment targets in DKA?
Blood ketones: falling by at least 0.5 mmol/L/h
Bicarbonate: rising by at least 3.0 mmol/L/h
Blood glucose: falling by at least 3.0 mmol/L/h
insulin should continue until - ketone measurement is less than 0.6 mmol/L,
venous pH over 7.3 and/or
venous bicarbonate over 18 mmol/L.
How is a low blood glucose treated while treating DKA?
If the blood glucose level falls below 14.0 mmol/L then 10% dextrose should be given at approximately 125ml/hr (8 hour bag)
How does potassium status change during DKA presentation and treatment?
Severe dehydration can lead to pre-renal acute kidney injury and transmembrane shifts in potassium due to the ketoacidosis. These collectively lead to hyperkalaemia. However, on initiation of insulin therapy plasma potassium concentrations dramatically fall leading to dangerous hypokalaemia.
What are the complications of DKA?
hypokalaemia adult-respiratory distress syndrome (ARDS) sepsis myocardial infarction cerebral oedema hypoglycaemia
What is Hyperglycaemic hyperosmolar state? Who does it occur in?
acute diabetic emergency that occurs in patients with type 2 diabetes mellitus.
Describe what Hyperglycaemic hyperosmolar state is characterised by
HHS occurs insidiously over several days with dehydration and metabolic disturbances
It is characterised by:
Hypovolaemia
Hyperglycaemia (> 30 mmol/L)
Mild or absent ketonaemia (blood ketones < 3 mmol/L)
High osmolality (> 320 mOsm/kg)
Which type of individuals usually develop Hyperglycaemic hyperosmolar state?
Patients are usually elderly with multiple co-morbidities, and as a result may be very unwell.
Can occur in younger patients
What are the counter regulatory hormones released when here is a lack of insulin?
cortisol, growth hormone, glucagon
