Diabetes emergencies Flashcards
How can we categorize diabetic emergencies
- ) Hyperglycaemic emergencies
2. )Severe hypoglycaemia
Outline hyperglycaemic emergencies
- ) DKA= diabetic ketoacidosis
2. ) HHS= hyperosmolar hyperglycaemic state ( previously known as HONK hyperosmolar non ketotic state)
What is DKA
- Complex disordered metabolic state due to absolute or relative insulin deficiency
- Mainly occurs in people with T1DM
- DKA defined by biochemical triad of
1. )hyperglycaemia
2. )Hyperketonaemia
3. )Metabolic acidosis
Diagnostic criteria:
- Blood glucose>11mmol/l or known diabetes
- Blood ketones>/= 3mmol/l or ketonuria>2+
- Bicarbonate<15mmol/l and/ or venous pH<7.3
How do our ketone levels increase?
- Lipolysis of our adipose tissue& triglycerides results in FAs which a processed by the liver to form ketones, so the as the amount of lipolysis occurs, so does the concentration of blood ketones
- Catecholamines, cortisol, glucagon & GH promote the production of FAs
What are some osmotic consequences of DKA
-dehydration
-Disordered potassium
This is due to osmotic diuresis
This can cause the release of stress hormones
What role can physiological stress have in the precipitation of DKA?
- Physiological stress results in stress hormones being released which leads to production of NEFAs which are partially oxidised by the liver and thus increases the concentration of ketones
- Stress hormones can also cause production of glucose by the liver
- Physiological stress can precipitate DKA in someone who’s still producing insulin or in someone who’s taking insulin
Explain the disordered potassium that occurs as an osmotic consequence of DKA
- Insulin causes K+ to move into cells usually
- In insulin deficiency K+ leaks out of cells leading to high EXTRAcellular K+ called hyperkalaemia
- Hyperkalaemia leads to renal k+ loss which leads to WHOLE BODY K+ depletion
- Acidosis has similar effects ( H+ & K+ compete)
What is ketonaemia?
Uncontrolled lipolysis and production of ketone bodies by the liver
- In the liver FA is partially oxidised to ketone bodies
- These ketone bodies are acetoacetate and 3-hydroxybutyrate and leads to acidosis
What happens to the K+ levels when DKA is treated?
-K+ moves rapidly into cells & because whole body k+ is deplete, extracellular k+ ( reflected in serum k+) falls very quickly
What could be the cause of DKA?
- Infection
- Acute illness
- Poor compliance
- Newly diagnosed
- Failure of care
- Unknown
What type of Diabetes is DKA classically associated with?
- To develop DKA you have to have absolute/relative insulin deficiency therefore its classically associated with people who have T1DM, so you would treat the patient as having T1DM until it’s proven otherwise
- Sometimes people with T2DM can still develop DKA
What are the complications of DKA?
- death
- cerebral oedema (decline conscious level)
- Adult respiratory distress syndrome/acute lung injury(due to fluid shifts)
- Pulmonary embolus (due to severe dehydration)
- Arrhythmias( due to K+ changes)
- Multi-organ failure (because your body has evolved to operate within quite a narrow pH & if you become acidotic everything starts to fail)
- Co-morbid states
What are the symptoms of DKA?
- Polyuria, polydipsia, thirst
- Weight loss
- Blurred vision( not from retinopathy, from fluid shifts in the lens in the eye)
- Vomiting
- Abdominal pain( due to ketones)
- Weakness
- Leg cramps (related to the hyperglycaemia; at this state there’s reduced glucose intake by muscle/fat and glucose is needed for the muscle to contract & relax properly. There is also a reduced amount of electrolytes due to increased excretion of glucose?)
Outline the signs of DKA
- Kussmaul respiration
- Ketotic factor
- Dehydration
- Tachycardia
- Hypotension
- Mild hypothermia
- Confusion, drowsiness, coma
What bedside tests can be performed when investigating DKA?
- CBG
- Blood ketones( portable ketone meters) or urine ketones
- Venous blood gases
What other investigations can be performed when investigating ketones
- Glucose/ U&Es( in testing for the electrolytes we are particularly looking for k+ & levels of dehydration
- FBC
- ECG
- CXR
- Blood culture
- MSU
What are the principles of DKA treatment?
- Fluid replacement (i.v 0.9% saline -normal saline)
- Insulin replacement ( Fixed rate i.v insulin infusion-0.1units/kg/hour)
- Potassium replacement (serum high but total body k+ low. once fluid & k+ is started, serum K falls rapidly; close monitoring of k+ is needed because a rapid drop will occur due to low total body k+)
- Identify and treat the cause ( may be an infection as the cause)
- Venous thromboembolism prophylaxis ( Low molecular weight heparin to reduce risk of getting a PE)
- Monitor in a high dependency unit( k+ may fall too rapidly; cerebral oedema may worsen due to i.v fluids; could put them in pulmonary oedema
