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    • Home
    • Welcome and Orientation
    • About This Guide
    • Patient Transfers
    • AAA
    • Anticoagulation Reversal
    • ARDS/Mechanical Vent
    • Atrial Fibrillation
    • Brain Death
    • CAR-T
    • Crash Cart/Defibrillator
    • CSW/SIADH
    • Cricothyrotomy
    • Cuff Leak. What is it?
    • Delirium/Antipsychotics
    • DKA/Other Ketoacidosis
    • EVD AND ICP MONITORS
    • ETOH Withdrawal
    • Extubation Readiness
    • Febrile Neutropenia
    • Fluids
    • GI Bleeds
    • Group A Streptococcus
    • Hypertension PRNs
    • Lido With Epi Recipe
    • Lines & Tubes on CXR
    • Lumbar Drains
    • Lung Volume Recruitment
    • Massive Transfusion
    • O2 Delivery Devices
    • Pacemaker Insertion
    • Pain/Analgesia
    • Pocket Pressor Recipes
    • Pulmonary Embolism/PERT
    • Respiratory Failure
    • ROSC
    • Sedation in ICU
    • Seizures/Status
    • Shock and Sepsis
    • Subarachnoid Hemorrhage
    • Swan Ganz Catheter Setup
    • TBI/EVD/ICP monitoring
    • TEVAR
    • Toxicology/Overdose
    • Tracheostomies AND THT
    • Trauma Patients in ICU
    • Tumor Lysis Syndrome
    • Vasoactive Medications
    • Ultrasound Guided Lines
  • Home
  • Welcome and Orientation
  • About This Guide
  • Patient Transfers
  • AAA
  • Anticoagulation Reversal
  • ARDS/Mechanical Vent
  • Atrial Fibrillation
  • Brain Death
  • CAR-T
  • Crash Cart/Defibrillator
  • CSW/SIADH
  • Cricothyrotomy
  • Cuff Leak. What is it?
  • Delirium/Antipsychotics
  • DKA/Other Ketoacidosis
  • EVD AND ICP MONITORS
  • ETOH Withdrawal
  • Extubation Readiness
  • Febrile Neutropenia
  • Fluids
  • GI Bleeds
  • Group A Streptococcus
  • Hypertension PRNs
  • Lido With Epi Recipe
  • Lines & Tubes on CXR
  • Lumbar Drains
  • Lung Volume Recruitment
  • Massive Transfusion
  • O2 Delivery Devices
  • Pacemaker Insertion
  • Pain/Analgesia
  • Pocket Pressor Recipes
  • Pulmonary Embolism/PERT
  • Respiratory Failure
  • ROSC
  • Sedation in ICU
  • Seizures/Status
  • Shock and Sepsis
  • Subarachnoid Hemorrhage
  • Swan Ganz Catheter Setup
  • TBI/EVD/ICP monitoring
  • TEVAR
  • Toxicology/Overdose
  • Tracheostomies AND THT
  • Trauma Patients in ICU
  • Tumor Lysis Syndrome
  • Vasoactive Medications
  • Ultrasound Guided Lines

dka and all cause ketoacidosis

Whether Ketoacidosis is caused by Type 1 Diabetes, an SGLT2 Inhibitor, Alcohol Ketoacidosis, Amphetamines, Pancreatitis, Type 2 Diabetes with Pancreatic Toxiciy, the can all be managed very easily and similarly with one approach.

MANAGEMENT OF ALL CAUSE KETOACIDOSIS

With only some small caveats (see individual scenarios below)

The most important issue is closure of the anion gap.  This is not a time to target glucose levels.


The diagram above is from Diabetes Canada and has been adapted specifically for ICU patients.  Follow this.  Some important issues to highlight:


  • You really cannot give insulin if the potassium is <3.3. .  Insulin is going to cause a shift of potassium into the cells and patients truly can arrest.  This is the main reason we do not bolus insulin up front.  Get the potassium running IMMEDIATELY.  Start it peripherally until you have a central line.  If they can swallow KDUR and not vomit it, give them some.  If they will tolerate an NG (mot of these patients are extremely agitated form their metabolic derangements), give them KCL Elixer.


  • You can start your insulin infusion as soon as the potassium is running, you just can't bolus is (in truth there is really no need to bolus it but in a patient with a higher potassium, you can, its not wrong)


  • Once the potassium is above 3.3, it is ok to give bicarbonate if the patient is severely acidotic and panting to compensate.  Bicarb is going to very transiently worsen the intracellular acidosis by increasing the CO2 and the patient will have to pant faster (see carbonic anhydrase equation below).  For patients who are fatiguing, they may not be able to rise to the occasion and so you will have to go slower to allow them to compensate.  


  • If they become hypoglycemic (although they should not with the instructions below), do not shut off the insulin.  Give them D50.


  • Once the anion gap is closed, you can either decrease your insulin to 0.5U/Kg or if they are less agitated and able to eat, you can give a dose of long acting SC insulin and then  safely discontinue your infusion in 2 hours.  Don't forget to also discontinue to the glucose infusion if they are eating.  


  • The SGLT2 Inhibitors have up to a 24 hour half life and so don't be too hasty in discontinuing insulin in them (see below)

CARBONIC ANHYDRASE EQUATION



There is no established protocol at the Ottawa Hospital that targets closure of the anion gap


There is no established protocol for ICU patients with DKA.  


Explicit Orders

  • Use the ICU Insulin order set


  • Delete the range and order a rate of 0.1 units/kg IV (example if the patient is 70kg, you will write a rate of 7 units of insulin/hr).


  • Indicate a starting dose (so for the same 70kg person the starting dose will be 7 units


  • Write "DO NOT TITRATE INSULIN" in the comments


  • D50 infusion with a range of 0-50cc/hr.  Write an order to titrate up or down by 10cc/hr to maintain glucose in a range of 7-9


  • Glucoscans much be hourly in order to maintain this


  • Patient will require an arterial line


  • DKA patients in the ICU often require central lines because of all the infusions of potassium, phosphate, often HCO3


  • If the patient is delirious be careful with your sedation - If the are in the ICU they are usually severely acidotic and they are tachypneic to maintain their pH from the ketones and lactate.  Sedation may drop their respiratory drive


  • Avoid intubating this patient for the same reason

TYpes of Ketoacidosis

Type 1 Diabetes

Pathophysiology

  • Bonafide deficiency or absence of insulin due to autoimmune destruction


Cause

DDX of presentation includes

  • first presentation (patient didn't know they had DM1)
  • non-compliance with insulin
  • illness (infection, stroke, MI) necessitating more insulin in the context of circulating cortisol and catecholamines
  • it is our job to investigate and sort this out


Caveats

  • usually require only a moderate amount of IV fluids.  They do not get as dehydrated because they do not have the same level of hyperglycemia to cause the osmotic diuresis


  • you do not have to bolus insulin but you can.  We are often in a scenario in the ICU where their potassium levels are so low that we really can't bolus insulin


Type 2 Diabetes (with Pancreatic Toxicity)

Pathophysiology

  1. Pancreatic Toxicity
  2. There are no insulin receptors in the pancreas.  Glucose is a "glucostat" for the pancreas meaning, it has to be allowed to come and go as it pleases in order to signal the pancreas as to how much insulin should be released 
  3. Prolonged exposure of the pancreatic beta cells to glucose causes an osmotic stress, inflammation, and toxicity
  4. The process is recoverable with treatment of the hyperglycemia


Caveat: 

  • often require insulin boluses for their hyperglycemia
  • Require more IV fluids than most other scenarios other than pancreatitis

Alcoholic Ketoacidosis

Pathophysiology

  1. Poor oral intake of nutrition
  2. Glycogen depletion
  3. Glucagon elevation
  4. Ketogenesis
  5. Additive stress of illness (2nd hit) with dehydration and increased cortisol/catecholamines
  6. Inability to increase glucose or insulin levels in the context of elevated glucagon
  7. hypoglycemic/euglyceic DKA


SGLT2-Inhibitors

The drugs that end in 'flozin" example Empagliflozin

Pathophysiology

  1. Glucosuria 
  2. Lower glucose in the blood stream decreases insulin secretion from the pancreas
  3. Lower glucose promotes upregulation of glycogen (diminished glycogen stores)
  4. Patient becomes sick and cannot compensate for elevated levels of cortisol and endogenous catecholamines by increasing glucose and therefore insulin levels particularly in the context of elevated glucagon and hence no glucose stores resulting in a euglycemic DKA


Caveat

  • These drugs have up to a 24 hour half life.  If you think you've fixed the problem and shut off the insulin in the first 24-48 hours there is a high likelihood that the DKA with recur


Adrenergic Stimulants

Pathophysioloy

  1. Supply and Demand (similar to the SGLT2-inhibitors)
  2. Constant state of adrenerngic upregulation (using glycogen stores)
  3. Usually malnourished (poor glucose stores in the first place)
  4. Low insulin levels (similar to SGLT2 inhibitors in that insulin is suppressed by glucose levels are low and glucagon has spiked to dip into stores
  5. New illness with increase in cortisol and endogenous catecholamines resulting in hypoglycemic/euglycemic DKA (akin to what happens in SGLT2 inhibitors)


Severe Pancreatitis

Two pathophysiologic possibilities 

  1. Pancreatic inflammation and toxicity which may recover 
  2. Bona fide beta cell destruction that may not recover (Requires ~90% of the pancreas to be destroyed before this occurs and results in true Type 1 DM


Caveats

  • They may require insulin boluses because they have the added issue of severe hyperglycemia due to inflammation


  • They require a lot of IV fluids


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