Diabetic ketoacidosis – T1-DM complication
- Uncontrolled catabolism due to insulin deficiency
- Children mortality due to cerebral oedema
- Adult mortality due to hypokalemia, ARDS, AMI
Pathology
- Hyperglycemia (>11mmol/L), hyperketonemia (>3mM), metabolic acidosis
- Hyperglycemia > osmotic diuresis > dehydration > Na/K loss
- Lipolysis > Free fatty acids > acetyl CoA > ketone bodies (mitochondria)
- Metabolic acidosis cause H+ into cells and K excretion
- Vomiting enhances water and electrolyte loss
Clinical features
- Kussmaul breathing , vomit, nausea, dehydration , hypotension, confusion, stupor
Diagnosis
- dipstick, bloods, hypokalemia, acidosis
- GCS , AVPU,
- Spirometry
Treatment
- Phase 1 Insulin [0.1U/kg/h]
- Saline/ potassium chloride (KCl)(20mg)
- pH(<7) – NaCO3 (1.26%), KCl(10mg)
- Phase 2
- Glucose (5% solution if <12mmol/L), KCl (20mg)
- Phase 3
- 4x daily insulin injections
- Need to administer KCl w/ insulin
- Glucose and insulin inhibits gluconeogenesis > inhibit ketone bodies
- Treat complications accordingly – coma, cerebral oedema (mannitol), hypothermia, DVT
Hyperosmolar hyperglycaemic state – T2-DM complication
- Severe hyperglycemia without ketoacidosis
- Hyper osmolality (>320mOsm)
- Absence of ketonemia (<3mM)
- Dehydration
- Glycosuria > osmotic diuresis
- Precipitated by AMI, infection, corticosteroids
Treatment
- Insulin (3U/h) , check plasma osmolality frequently
- Prophylactic anti-coagulants
- Fluids
Hypoglycaemia – T1-DM treatment complication
- BGL – <3.5mmol/L
- Commonly due to insulin therapy
Healthy people (feedback for low BGL)
- Insulin secretion supressed > glucagon secreted > catecholamines secreted (ANS) > gluconeogenesis
- Exogenous insulin cannot be regulated in the body
Clinical features
- ANS – sweating, tremor, palpitations, hunger, anxiety
- Neurological – confusion, drowsiness, speech
- Nausea, headache, drowsiness
Treatment
- Carbohydrates, glucose, dextrose, mannitol (cerebral edema)
- I.V/I.M – if unconscious, oral if conscious