Diabetic Emergencies

DKA

Diabetic Ketoacidosis is a Triad

  1. ketonaemia: ++ urine or >3mmol/l
  2. hyperglycaemia: >11mmol/l
  3. acidaemia : pH<7.3 or bicarb <15mmol/l

Characterisations

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

Pathophysiology

  • 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

Controversies in management

  • 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.

Complications

  • 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

Management

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

Baseline investigations:

  • electrolytes, Full blood, Lactate, VBG, Glu, urinalysis

Further Ix depending on likely cause:

  • stool MCS, urine MCS, blood cultures, CXR, CT
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.

management-of-dka-241013.pdf
condensed_adult_diabetic_ketoacidosis_dka_management_chart_aug_2017.pdf
dka_and_hhs_prescription_jbds_april_2018_.pdf
Jt Brit Soc Diabetes guidelines DKA 2021

Hyperosmolar Hyperglycaemic State

References include:

wiki/endocrine/diabetic_ketoacidosis_dka.txt · Last modified: 2023/04/25 14:16 by 127.0.0.1
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