=====Diabetic Emergencies=====
====DKA====

=== Diabetic Ketoacidosis is a Triad ===

  -ketonaemia: ++ urine or >3mmol/l
  -hyperglycaemia: >11mmol/l
  -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 (<wrap em>FIII is current standard</wrap>)
  *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


[{{  :wiki:endocrine:dka.png?400|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 <wrap em>constant, fixed rate IV infusion is the mainstay of treatment</wrap>, 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.

{{ :wiki:endocrine:management-of-dka-241013.pdf |}}\\ 
{{ :wiki:endocrine:condensed_adult_diabetic_ketoacidosis_dka_management_chart_aug_2017.pdf |}}\\ 
{{ :wiki:endocrine:dka_and_hhs_prescription_jbds_april_2018_.pdf |}}\\ 
{{ :wiki:endocrine:jbds_02_dka_guideline_amended_v2_june_2021.pdf |Jt Brit Soc Diabetes guidelines DKA 2021}}\\ 


====Hyperosmolar Hyperglycaemic State====

{{ :wiki:endocrine:jbds_ip_hhs_adults.pdf |Jt Brit Diabetes soc - guidelines for HHS 2012}}\\ 

===References include:===
https://www.diabetes.org.uk/resources-s3/2017-09/Management-of-DKA-241013.pdf \\   
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4085289/ \\  
http://www.lhp.leedsth.nhs.uk/detail.aspx?id=882  \\