Become the expert in the diagnosis and management of Diabetic Ketoacidosis!
Need to close a major “gap” in your Diabetic Ketoacidosis knowledge? Look no further than our conversation with diabetes expert and repeat guest, Dr. Hussein Abdullatif, a dedicated multiple-award-winning clinician-educator at UAB. Join us as Dr. Abdullatif walks us through the diagnosis, management, and social implications surrounding DKA.
- Producer, Writer, & Infographic:: Shannon Snellgrove
- Cover Art: Christopher Chiu MD
- Hosts: Justin Berk MD and Christopher Chiu MD
- Editor:Justin Berk MD; Clair Morgan of nodderly.com
- Guest(s): Hussein Abdullatif MD
- It should be goal to catch the diagnosis of Diabetes before the patient presents in DKA
- Patients with DKA can appear to be maintaining their urine output due to the osmotic diuresis, but they are actually very volume down
- The pH can be falsely reassuring when the patient has a concurrent contraction alkalosis
- Along with ketosis, there is often a concurrent lactic acidosis
- While there can be contributing triggers to DKA (ie infection causing increased metabolic rate), the overarching cause of DKA is lack of insulin
- There has been no evidence to suggest a difference in neurologic outcomes from using 0.45% NaCl vs 0.9% NaCl as the resuscitative fluid
- Insulin is given to correct the acidosis, not bring down the hyperglycemia
- When transitioning from insulin drip, subcutaneous insulin should be given before stopping the drip due to insulin’s short half-life (or else the acidosis will come back!)
- Patients in DKA due to type 2 diabetes can be at higher risk for developing hypophosphatemia and subsequently rhabdomyolysis
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DKA Diagnostic Criteria
Diagnosis of DKA is based on the biochemical triad of ketonemia, hyperglycemia, and acidemia along with a diagnosis of diabetes. (ISPAD Clinical Practice Consensus: DKA, 2018)
- Ketonemia (blood β-hydroxybutyrate ≥3 mmol/L) or moderate or large ketonuria
- Hyperglycemia (blood glucose >11 mmol/L [~200 mg/dL])
- Venous pH <7.3 or serum bicarbonate <15 mmol/L
- Expert opinion: some providers deem a bicarbonate <18 as acidemic, but Dr. Latif usually waits until bicarbonate is <15 to pull the trigger on starting an insulin drip
Presentation of DKA
The presentation of DKA can vary greatly depending on the timing and severity of illness. Often begins with symptoms of diabetes (polyuria, polydipsia, loss of weight).
The “benign” presentation
DKA can often present very mildly if in its initial stages. Often with nausea/vomiting, vague abdominal pain, but adequate urine output. Patients with DKA can appear to be maintaining their urine output due to the osmotic diuresis, but they are actually very dehydrated. Be concerned if the patient presents with weight loss as well. Children should not be losing weight, this should almost always be taken as a warning sign. Additionally, if a child presents with nausea/vomiting but no diarrhea, make sure to ask “is this really simple gastroenteritis?” Checking a urinalysis and/or glucose are easy and cheap tests to help rule out DKA in a clinic setting when patients present with this benign presentation.
- The urinalysis: While you should expect to find ketones in the urine of someone who has been vomiting for multiple days; you should not expect glucose. If there is glucose and ketones in urine, even without drawing blood you can know there is something significant going on.
The “severe” presentation
In its later stages, DKA will present with signs and symptoms related to compensating for the metabolic derangement.
- Hyperventilation and deep (Kussmaul) breathing (compensation for metabolic acidosis)
- Signs of intravascular volume depletion (tachycardia, poor skin turgor, poor peripheral perfusion
- Neurologic findings ranging from drowsiness, lethargy, and obtundation to coma mainly related to degree of acidosis
Explaining the diagnosis
- Patients are often very sick when presenting in DKA, it may be best to just gauge where the patient or caregiver is at in terms of their anxiety level at that time. It may note be a time to talk in great detail explaining the diagnosis, but just to support and reassure them without giving false hope.
- “Because of the patient’s diabetes and the lack of insulin, the body has accumulated acid in their system and that acid is playing a role in making them sick. We are in a critical situation, but we are very hopeful we will come out of it by using insulin and fluids.”
- It is important to pay attention to the caregiver’s sense of guilt that may be present
- If it is a new diagnosis of diabetes, it is not necessarily important to deem the patient as having type 1 or type 2 diabetes. What is important at that time is that they need insulin.
What makes DKA so scary?
- Potential mortality of DKA is 4-6%
- Potential causes of mortality
- The anion gap is due to the build-up of ketones, but there can also be a concurrent lactic acidosis that is contributing
- The characteristic Kussmaul breathing (deep and rapid breathing) occurs to clear CO2 in order to correct the acidosis
- Brain edema
- Can be due to DKA itself and/or treatment
- Electrolyte imbalances
- The pH can be falsely reassuring when the patient has a concurrent contraction alkalosis from dehydration
- After giving fluids, the pH can transiently worsen before it gets better
- There is a build-up of acid inside the cells and after rehydrating the acid can come out and worsen the acidosis
- A VBG is usually sufficient in DKA as long as pulse oximetry is reliable. Oxygenation is usually not a concern in DKA. (Farkas 2016)
What triggers DKA?
- The overarching thing that happens is that the patient has an inadequate amount of insulin (and therefore they are not using glucose and resort to using fats as a source of energy).
- Expert opinion: There is a theory that with the lack of insulin, we increase the production of glucagon. The increased glucagon increases gluconeogenesis which results in even more un-usable glucose fat breakdown and accumulation of ketones.
- There are known triggering factors for the development of DKA due to the increase in the basal metabolic rate in addition to inadequate insulin therapy
- Infection and acute coronary/vascular event are the most common (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6771342/)
- There does not have to be a triggering factor present for a patient to go into DKA. The overarching cause of DKA is lack of insulin.
When to send to the ICU
- Tends to be center-dependent, but some common criteria for admission to ICU for DKA include
- Age <2
- pH <7.1
- If the patient received insulin as a bolus in an outside facility
- Every patient with DKA needs one-on-one nursing due to the need for an insulin drip
The 3 Pillars of Treatment
- The general consensus is to use isotonic fluids (0.9% NaCl) for resuscitation.
- 0.45% NaCl is not isotonic, but once electrolytes are also added it becomes close to an isotonic solution.
- Lactated Ringers are also used with the idea being less chloride being pushed, as chloride itself can be a cause of non-anion gap metabolic acidosis.
- Expert opinion: Start off the fluid resuscitation with 0.9% or LR and transition to 0.45% with electrolytes later on. In terms of the amount of fluids, Dr. Latif calculates the amount as if the patient is 10% volume down with the correction for 10% happening over 48 hours. It is dehydration, but more importantly this is a hyperosmolar dehydration so correction should happen slower.
- There has been no evidence to suggest a difference in the risk of the developing cerebral edema when comparing 0.9% NaCl vs 0.45% NaCl as the resuscitative fluid.(Kupperman 2018)
- When should we add dextrose to the fluids?
- If the glucose is dropping at a fast rate ( >100mg/dL/hr)
- The osmolarity in the blood is dropping quickly but the osmolarity in the brain is not dropping that quickly, which is worrisome for the development of brain edema
- If the blood glucose is 250-300
- When should we consider giving bicarbonate?
- Used very sparingly. Only consider if concerned about organ failure occurring due to the acidosis.
- Insulin is often not administered immediately as the glucose may drop substantially just with fluids alone due to volume expansion.
- Dr. Latif advises to give fluids for ~1 hr and then start the insulin.
- If giving insulin through a drip, it is a set dose (0.1u/kg/hr with a max of 100 kg).
- This high-dose insulin is needed in DKA due to needing more insulin to overcome the amount of insulin resistance present.
- Why are we giving the insulin?
- To correct the acidosis! While the insulin will bring down the glucose, we are most concerned with correcting the acidosis. Without insulin, the acidosis will come back!
- When can we stop the insulin drip?
- When the bicarbonate is >15. Stopping the insulin should not be determined by the glucose.
- It’s important to keep in mind that insulin has a short half-life (7-10 minutes), so when you want to stop an insulin gtt, subQ insulin should be given before you stop the drip or right at the time of stopping the drip.
- There is a new movement starting of giving basal insulin at the time of presentation along with starting the insulin drip. This gives a safety level of insulin, so there is less worry when stopping the insulin drip. (Barski 2018)
- Electrolytes should be checked at least every 4 hours
- The electrolyte we are most concerned about is K. In DKA, patients can present with high K which may make us less likely to give K due to concern for hyperkalemia. However, once we start treating DKA, the K will drop.
- If you did not initially give K, check lytes every 2 hours so make sure the patient doesn’t develop hypokalemia.
- When to add K to the drip is center-dependent, but common criteria is to add K when K is <5.5
- Absolute contraindications to giving K are EKG abnormalities or no urine output
“Ketosis prone” Type 2 Diabetes
- Traditionally, DKA is associated most with Type 1 Diabetes, however, DKA can happen in all types of diabetes.
- DKA that happens with type 2 diabetes has likely been present for longer and can present with additional risks due to this
- Patients in DKA with type 2 diabetes are more likely to have hypophosphatemia, which puts them at higher risk for rhabdomyolysis
- SGLT2 inhibitors (empagliflozin, canagliflozin, dapagliflozin) lower the threshold for losing glucose in the urine and therefore they lower the average glucose level
- Patients then require less insulin overtime due to lower average glucose levels which can ultimately lead to developing DKA without high blood glucose
- If using these medicines, make sure to educate patients on how to be vigilant on avoiding developing ketosis
- Treatment of euglycemic DKA includes starting an insulin drip and dextrose-containing fluids simultaneously
- It is important to think about all of the social factors that can be contributing to why a patient develops DKA. Always attempt to address the underlying issue of their current diabetes regimen and connect with resources to help remedy the issue if possible.
- Examples such as needle phobia, reliable caregivers to administer insulin, trouble with calculating correct insulin dosing, monetary/insurance issues, etc.
Listeners will understand the presentation, work-up, and management of Diabetic Ketoacidosis. Additionally, listeners will recognize many of the social determinants of health that contribute to the development of DKA in patients with diabetes.
After listening to this episode listeners will… .
- Recognize the constellation of symptoms that occur in DKA
- Utilize appropriate work-up in the diagnosis of DKA
- Comprehend the reasoning behind the mainstays of treatment of DKA
- Be confident in managing DKA
- Identify the social determinants of health that correlate with increased incidence of DKA (how important social work and child life can be in these patients)
Dr Abdullatif reports no relevant financial disclosures. The Cribsiders report no relevant financial disclosures.
Snellgrove S, Abdullatif H, Chiu C, Berk J. “#22: DKA: Mind the Gap!”. The Cribsiders Pediatric Podcast. https:/www.thecribsiders.com/ March 31, 2021