Diabetic ketoacidosis (E&M) Flashcards
Define DKA.
Acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment
Who does DKA occur in and why?
T1DM patients –> no insulin to suppress lipolysis –> ketone formation –> acidosis
What may DKA indicate?
Initial presentation in someone with undiagnosed T1DM
(DKA is the most common acute hyperglycaemic complication of T1DM)
Why does ketogenesis occur in DKA?
Excessive glucose but insufficient insulin to push it into cells –> body goes into a starvation-like state where ketogenesis is the only mechanism of energy production
What are some precipitating/contributing factors to DKA?
- most common: infection + discontinuation of/inadequate insulin therapy
- underlying medical conditions e.g. MI or pancreatitis
- drugs affecting carbohydrate metabolism e.g. corticosteroids, thiazides, sympathetic agents
- SGLT-2 inhibitors
What are the sick day rules for T1DM patients? (4)
- continue normal insulin dose
- check BGC more regularly
- drink 3L of fluid over 24h
- self-monitor ketones regularly throughout day
What is DKA a biochemical triad of?
- hyperglycaemia
- ketonemia
- metabolic acidosis
(With rapid symptom onset)
What are the clinical features of DKA? (9)
- diabetic features (polydipsia, polyuria, weight loss, tiredness)
- nausea & vomiting
- abdominal pain
- dehydration (dry mucous membranes, decreased skin turgor, slow CRT, tachycardic, hypotensive)
- hyperventilation (Kussmaul breathing)
- reduced consciousness
- hypothermia
- ketotic breath (acetone smell/fruity)
- rapid onset (<24 hours)
What might you see on examination in DKA? (5 - overlap with clinical features)
- dehydration (dry mucous membranes, decreased skin turgor, slow CRT, tachycardic, hypotensive)
- hyperventilation (Kussmaul breathing)
- reduced consciousness
- hypothermia
- ketotic breath (acetone smell/fruity)
What are the signs of dehydration in DKA? (5)
- dry mucous membranes
- reduced skin turgor
- slow capillary refill time
- tachycardia (with weak pulse)
- hypotension
Why does Kussmaul breathing occur in DKA?
Decrease in pH stimulates respiratory centre to try and correct acidosis by blowing off CO2 –> deep, rapid, laboured breathing
What are some risk factors for DKA? (6)
- infection (most common precipitating factor)
- inadequate insulin therapy
- undiagnosed T1DM
- MI (or pancreatitis)
- drugs affecting carbohydrate metabolism e.g. corticosteroids, thiazides, sympathetic agents
- SGLT-2 inhibitors
Why is infection the most common precipitating factor for DKA?
- increased cortisol in infection (antagonist of insulin) –> body’s insulin requirements increase
- T1DM patients should make sure they continue taking insulin when unwell to prevent DKA
What are the first-line investigations for DKA? (5)
- venous blood gas (VBG)
- blood ketones (high)
- blood glucose (high)
- U&Es
- FBC (raised WCC without infection)
What does VBG show in DKA? (4)
- metabolic acidosis with raised anion gap (>16 indicates severe DKA) with partial respiratory compensation (hyperventilation)
- pH <7.0 indicates severe DKA
- hyperkalaemia is common (replace K+ if <5.5)
- high plasma osmolality (>320mmol/kg)
What do U&Es show in DKA? (3)
- hyponatraemia and hyperkalaemia are common due to lack of insulin
- hypokalaemia is an indicator of severe DKA
- may show hypomagnesaemia and hypophosphataemia
What investigation is done if severe DKA?
ECG - MI, hypokalaemia (U waves) or hyperkalaemia (peaked T waves)
How does alcoholic ketoacidosis present differently to DKA and how is it managed? (1 + 2)
- low or normal glucose levels (vs high)
- rehydration with IV saline 0.9%
- thiamine to prevent Wernicke’s encephalopathy
What are some differential diagnoses for DKA? (7)
- hyperosmolar hyperglycaemic state (T2DM, glucose>33.3mmol/L, normal urine ketones)
- lactic acidosis (normal serum glucose and ketones, elevated serum lactate)
- starvation ketosis
- alcoholic ketoacidosis (occurs when alcohol and caloric intake decreases)
- salicylate poisoning
- ethylene glycol/methanol intoxication
- uraemic acidosis
What is the diagnostic criteria for DKA? (4)
All 4 needed:
- acidaemia (pH<7.3)
- hyperglycaemia (>11mmol/L)
- ketonemia (>3mmol/L)
- bicarbonate (<15mmol/L)
What are the key parts to DKA management?
- fluid replacement
- insulin (reduce ketones)
- correction of electrolyte imbalances
How do we manage fluid replacement in DKA?
- most patients with DKA deplete around 5-8L
- isotonic saline used initially, even if patient severely acidotic
- if SBP<90mmHg - 500ml bolus saline over 10-15min (if no response give second bolus)
- if SBP>90mmHg / response to first bolus - start 1L 0.9% NaCl over 1 hour
- add KCl to second litre of IV fluids
What do you give if pH<6.9 in DKA?
Sodium bicarbonate
How do we manage insulin replacement in DKA?
- fixed-rate IV insulin infusion started at 0.1 units/kg/hour (50U soluble insulin in 50mL normal saline)
- once BGC <15mmol/L, add 10% dextrose
- if capillary ketones <0.3, pH>7.3 or HCO3>18, use SC insulin instead (however there must be overlap between IV and SC insulin for 1-2h)
What do we do with existing insulin medication in DKA?
Continue long-acting insulin, stop short-acting insulin
How do we correct electrolyte disturbance in DKA?
- serum K+ often high on admission despite total body K+ being low
- this often falls quickly following treatment with insulin (as insulin drives K+ into cells) –> hypokalaemia –> potassium replacement
- if the rate of potassium infusion >20mmol/hr, then cardiac monitoring may be required
What are the signs of DKA resolution (within 24h), and what do we do if this has not happened? (3 + 1)
- pH>7.3 and
- ketones <0.6mmol/L or <2+ urine dip and
- bicarbonate >15mmol/L
If has not resolved: refer to senior endocrinologist
What are some complications of DKA itself (not iatrogenic)? (5)
- gastric stasis
- thromboembolism
- arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
- ARDS
- AKI
What are some iatrogenic complications from incorrect DKA fluid therapy? (3)
-
cerebral oedema (children/young adults)
- headaches
- reduced consciousness
- rise in BP
- seizures
- hypokalaemia
- hypoglycaemia
