wiki:endocrine:diabetic_ketoacidosis

Diabetic Emergencies

typical losses
- water: 100/kg
- Na+: 7-10mmol/kg
- Cl-:3-5mmol/kg
- K+: 3-5mmol/kg

Insulin deficiency, increased insulin counter-regulatory hormones (cortisol, glucagon, growth hormone, and catecholamines), and peripheral insulin resistance lead to hyperglycemia, dehydration, ketosis, and electrolyte imbalance
increased lipolysis and decreased lipogenesis, abundant FFA's are converted to ketone bodies: β-hydroxybutyrate (β-OHB) and acetoacetate.
Hyperglycemia-induced osmotic diuresis causes dehydration, hyperosmolarity, electrolyte loss, and subsequent decrease in glomerular filtration rate
reduced renal function leads to reduction in glycosuria and hyperglycemia worsens
impaired insulin action and hyperosmolar hyperglycemia leads to reduction in K+ uptake by skeletal muscle
hyperosmolarity causes efflux of K+ from cells leading to intracellular K+ depletion and loss of K+ via osmotic diuresis

Arterial or venous measurements - difference between venous and arterial pH is 0.02-0.15
blood ketone measurement - whilst high levels of ketones might not give consistent results,these levels are still well above the levels needed to diagnose and manage DKA
Colloid versus crystalloid - critical care consensus suggests that colloids should be avoided where possible due to a potential risk of increased mortality and morbidity
Rate of fluid replacement - concern that rapid fluid replacement may lead to cerebral oedema in children and young adults, hence caution in this group
0.9% sodium chloride vs Hartmann’s - no agreement but saline generally used with added K+
Continuation of long-acting insulin analogues and basal human insulins - avoids rebound when IV insulin is stopped
Fixed-rate IV insulin infusion (FRIII) versus variable rate IV insulin infusion (FIII is current standard)
Initiating treatment with a priming (bolus) dose of insulin - unnecessary
IV bicarbonate - Excessive bicarbonate may cause a rise in the pCO2 in cerebrospinal fluid (CSF) and may lead to a paradoxical increase in CSF acidosis. IV bicarb may delay fall in lactate:pyruvate ratio and ketones. Some suggestion that Bicarb use may be implicated in cerebral oedema young patients.
Use of intravenous phosphate - no evidence of benefit in replacing quite significant losses unless signs
rate of glucose lowering - low dose insulin infusion appears to lower glu at similar rate to high dose IV infusion once used.

hypo and hyperkalaemia
hypoglycaemia - if not watched and fall in Glu is monitored. Rebound ketosis driven by counter-regulatory hormones may result
cerebral oedema - uncommon in adults
- Iatrogenic vs present before?
- Especially in children
- Especially if Bicarb given
pulmonary oedema - rare
- iatrogenic
- Especially in elderly and those with cardiac dysfunction

Underlying causes must be at the forefront of examination and investigation.

Baseline investigations:

Further Ix depending on likely cause:

Summary of fluid, K+ and Insulin regimens in treatment of DKA

Treatment strategy (see diagram):

N saline - fluid of 1st choice and rate is dependent on initial sBP and response
Insulin - baseline long acting insulins will continue but a constant, fixed rate IV infusion is the mainstay of treatment, only altering if poor response to hourly goals. Insulin commences after fluid resuscitation commences.
K+ replacement - generally not in 1st hour but then according to value. Must be above 3.3 before insulin commences
Fluid management and management of ketosis and Glucose control are central to recovery.
Fluid management pathways are a baseline. A proper assessment of fluid status requires a thorough examination
ECF volume assessment is based on physiological signs - HR, BP, UO, CVP etc
- UO should exceed 0.5ml/kg/hr
TBW is assessed biochemically - osmolarity, Na+
reviews must be carried out regularly, hourly at 1st, to assess progression of recovery and to alter management if needed.
- Ketosis should reduce at rate: 0.5mmol/L/hr
- Bicarb should rise at rate: 3mmol/L/hr
- Glu should fall at rate: 3mmol/L/hr
urinary catheter and CVC lines may be required
address precipitating factors
conversion to appropriate subcutaneous insulin when biochemically stable (blood ketones less than 0.6mmol/L, pH over 7.3)and the patient is ready and able to eat.