Diabetic ketoacidosis Flashcards
Clinical features of DKA
Gradual drowsiness, vomiting, dehydration (headache, seizures, dry mucous membranes) in T1DM Abdo pain Ketotic breath Polyuria, polydipsia Lethargy Anorexia Coma Deep rapid breathing - Kussmaul’s hyperventilation
What is the mechanism of DKA?
Lack of insulin and elevation in glucagon leads to release of glucose by the liver via glycogenolysis and gluconeogenesis. Blood glucose rises and spills over into urine resulting osmotic diuresis –> polyuria, dehydration and polydipsia. Ketoacidosis is an alternative metabolic pathway to produce energy from fatty acids in starvation states. It produces (acetone, acetoacetate, beta-hydroxybutyrate) acidic ketone bodies, as a byproduct - hence fruity breath smell. Body initially buffers with bicarbonate but this is overwhelmed so compensatory hyperventilation to lower blood CO2 - compensatory resp alkalosis - Kussmaul respiration. In DKA, there is excessive glucose but because of lack of insulin this cannot be taken up into cells to be metabolised so pushing the body into a starvation like state where ketoacidosis is the only mechnism of energy production. Body water falls due to rise in blood sugar and resistance to insulin increases further. Combination of metabolic acidosis and hyperglycaemia can be deadly.
What are triggers of DKA?
Infection Not taking insulin correctly/non-compliance stroke MI Panceratitis Surgery Chmotherapy Antipscyhotics
How is DKA diagnosed?
Acidaemia pH < 7.3 or HCO3 < 15 Hyperglycaemia BM > 11mmol/L or known DM Ketonaemia (3mmol/L or more) or significant ketonuria (2+ on dipstick)
What is immediate management for DKA and where should patients be managed?
If systolic BP < 90 then give 500ml bolus over 15 mins and reassess - if still , 90 seek senior help IV fluids 0.9% saline (hypotonic compared to plasma) 1L over 1hour Include potassium chloride in fluid unless anuria is suspected - adjust according to plasma potassium concentration. Insulin intravenous infusion with 0.9% saline 1unit/ml. Infuse at 0.1units/kg/h Continue established long-acting SC insulin Antibiotics in underlying infection
What investigations for DKA?
Bedisde: ECG, CXR, BP, RR, Urinalysis - dipstick and MSU
Bloods: ABG, VBG, Ketonuse, capillary glucose, FBC, CRP, U&E, amylase/lipase, culture
Imaging CT head if cerebral oedema
How do you assess patients response to treatment? How long should you continue?
Monitor blood ketone and blood glucose concentrations and adjust insulin infusion rate accordingly Blood ketone concentration should fall by 0.5mmol/l/h and blood glucose should fall by 3mmol/L.hour Once glucose < 14mmol/L start 10% glucose by IV infusion at 125ml/hour to avoid hypoglycaemia. Continue insulin until ketone < 0.6mmol/L, pH > 7.3 and bicarb > 15mmol/L
When would you put patient back on SC insulin?
Established subcutaneous therapy with long-acting insulin analogues (insulin detemir or insulin glargine) should be continued during treatment of diabetic ketoacidosis. Continue insulin infusion until blood-ketone concentration is below 0.3 mmol/litre, blood pH is above 7.3 and the patient is able to eat and drink; ideally give subcutaneous fast-acting insulin and a meal, and stop the insulin infusion 1 hour later.
What are complications of treatment?
Hypokalaemia Cerebral oedema - Overvigorous fluid replacement - swelling of brain, decreased blood flow, death - That with artificial ventilation and IV mantel and hypertonic saline to reduce swelling ASpiration penumonia
What steps to prevent DKA?
Sick day rules for diabetics Education about triggers Instructions on how much extra insulin to take when sugar levels appear uncontroled Easily digestible diet rich in salt and carbs when ill Means to suppress fever and treat infection Call for medical help Evaluate insulin use and compliance Monitor own ketone level
