Links To And Excerpts From The Curbsiders’ #331 Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS) with Dr. Dave Lieb

In this post, I link to and excerpt from The Curbsiders  #330 & #331 Inpatient Diabetes with Dr. Dave Lieb

The above are two episodes placed on one web page.

In this post I link to and review #331 Inpatient Diabetes Part 2: DKA, insulin drips, insulin pumps, and CGMs.

In yesterday’s post, I reviewed #330 Inpatient Diabetes Part 1: Insulin regimens, oral hypoglycemics, corrections scales and more! with Dr. Dave Lieb.

All that follows is #331 Inpatient Diabetes Part 2: DKA, insulin drips, insulin pumps, and CGMs.

More inpatient diabetes! In this part 2 of 2, we cover diabetic ketoacidosis (DKA), euglycemic DKA, how to handle insulin pumps in the hospital, continuous glucose monitors, and how to transition patients off an insulin drip! Our guest is Dr. Dave Lieb (@dclieb), an internist, endocrinologist and the endocrinology program director from Eastern Virginia Medical School.

Show Segments
  • Intro
  • DKA and HHS – introduction and therapy overview
  • Insulin drips, closing the gap and transitioning to a subcutaneous regimen
  • Euglycemic DKA
  • Pumps and glucose monitors
  • Final take home points
  • Outro

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Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS)

DKA Basics

DKA is defined as being the presence of acidosis (arterial pH < 7.30), in association with hyperglycemia (serum glucose > 250 mg/dL) along with urine and serum ketones [Kitabchi et al 2009]. It is further classified as mild, moderate or severe based on the degree of laboratory derangement and the patient’s mental status. Additionally, there exists a related condition – HHS which typically presents in patients with very high blood sugar (>600 mg/dL) in the absence of acidosis. Dr. Lieb states that a major discriminating factor is how much insulin is “around.” Specifically, he reminds us that many patients with HHS suffer primarily from dehydration and that a significant degree of the patient’s hyperglycemia can be managed by fluid resuscitation.

Therapy Pearls

IV insulin therapy is a mainstay of DKA care. Therefore these patients often benefit from admission to an intensive care unit. These patients are generally very dehydrated and thus, need significant fluid resuscitation. Often, the dehydration (glucosuria causing an osmotic diuresis) is associated with hypokalemia which requires aggressive management. Dr. Lieb recommends avoiding normal saline to avoid the hyperchloremic acidosis that it can cause. From a pathophysiology standpoint, patients either have an absolute or relative insulin deficiency (i.e. ketosis prone type 2 diabetes). Due to the insulin deficiency, these patients have a rise in serum glucagon which causes free fatty acid conversion into ketone bodies.

Sometimes DKA occurs due to a lack of insulin (i.e. a patient fails to take sufficient  insulin for whatever reason). However, often DKA is precipitated by infection or some other stressor such as an acute MI, a progressive wound or trauma. Determining the precipitating factor for DKA is just as important as treating it! Dr. Lieb cautions us against the major pitfall of assuming a patient’s presentation is due to “non-compliance.” In fact he advocates against the use of that term – as do we at The Curbsiders – since there is always a reason for treatment failure that can and should be identified. This is especially important in patients who are frequently admitted to the hospital with DKA. From a pathophysiology, it seems that many of these stressors share a common pathway – i.e. the production of pro-inflammatory cytokines – which leads to derangements of glycemic control [Palmero et al 2020].

Treatment is generally protocolized, and these protocols are determined at the hospital level.

It is imperative that, despite such protocols, clinicians still need to be vigilant in case the protocol is not adequately treating the patient. Alternatively, some patients may have mild DKA (pH>7.25, serum bicarbonate of 15-18 mEq/L, glucose > 250 mg/dL) and do not need insulin drip management but instead could be managed via subcutaneous insulin. Dr. Lieb references this recent paper in the Journal of Clinical Endocrinology and Metabolism that can help clinicians triage DKA severity [Palmero et al 2020]. As a bonus, this article discusses DKA in the era of COVID-19! In systems where ICU resources may be limited, this approach provides a means to manage mild DKA in the general medicine wards.

In regards to treatment goals, Dr. Lieb discusses a few measurables. Some providers will measure serum ketones and look for a downtrend. Monitoring electrolytes (especially potassium and phosphate) is very important. Perhaps more important than labs, is the patient. Are they in pain or bedbound? Or are they feeling better and developing an appetite?

Transitioning from the Drip 

The transition from insulin drip to subcutaneous insulin may be the most critical part of a patient’s hospitalization. Dr. Lieb implores us to make sure the patient feels better and has an appetite prior to stopping the drip. Additionally, he recommends electrolyte derangements should be treated, the patient should not be acidotic, have a normal anion gap and have a serum bicarbonate > 18 mEq/L. When transitioning, Dr. Lieb explains that the patient should receive basal insulin while on the drip, with a goal of a one to two hour overlap, prior to cessation of the drip. Once the patient’s food has arrived, the drip can be turned off (assuming that overlap occurred!) and then the patient should eat and receive their first dose of meal time insulin with any correctional insulin if indicated.

How much insulin should the patient be on? Dr. Lieb recommends looking at the last 4-6 hours while the patient was “NPO” and on the drip. This number, extrapolated over 24 hours (i.e. x4 or x6) gives a rough estimate of the patient’s basal needs. Doubling that amount is a rough estimate of their daily needs, allowing the clinician to devise a basal bolus strategy tailored to the patient. Some clinicians will be more cautious and multiply the calculated total daily insulin dose by 0.8, but this is clinical-dependent.

What About Euglycemic DKA?

Most patients with DKA will have a blood glucose > 250 mg/dL, however, 5% of patients with DKA will have a blood glucose that is either euglycemic or less than 200 mg/dL [Long et al 2021]. In euglycemic DKA, the pathophysiology differs from hyperglycemic DKA in that there is a combination of a relative insulin deficiency with a concurrent glucose deficiency. This could be seen in pregnant patients, malnourished patients, patients with liver disease or who suffer from alcohol use disorder, for example. A common scenario that clinicians need to be aware of relates to the use of SGLT-2 inhibitors. These agents work by increasing glucosuria to reduce serum blood sugar. A patient who, for example, has developed sepsis from an infection but has continued their SGLT-2 inhibitor, is set up for developing euglycemic DKA, thereby complicating their clinical course. Should a patient who develops euglycemic DKA stop their SGLT-2 inhibitor? In Dr. Lieb’s expert opinion, these drugs are effective and it may be reasonable to continue them, especially if the patient has a strong indication such as concomitant heart disease or renal failure. Any patient on an SGLT-2 inhibitor should be cautioned to hold the drug in certain circumstances, such as during illness, when fasting, or during the perioperative period (Goldenberg 2016).

From a treatment standpoint, while these patients may not need aggressive insulin therapy for hyperglycemia management, they do require aggressive hydration and electrolyte management. They still require insulin in order to close their anion gap and treat ketosis. Due to their euglycemia, they may require more dextrose to prevent hypoglycemia than those with hyperglycemic DKA. Overall,  Dr. Lieb cautions providers against missing these patients who have a reassuring blood sugar but otherwise need the same level of vigilance as classic DKA patients.

Insulin Pumps

Pumps 101

Insulin pumps are great… except when they fail! Dr. Lieb suggests that we counsel any of our patients with insulin pumps to be on the lookout for symptoms of hyperglycemia. If a patient feels malaise, fatigue or other symptoms without an obvious cause, he recommends a finger stick to check blood sugar, followed by insulin injection if indicated, rather than trying to troubleshoot the pump. This is a good way to prevent symptomatic hyperglycemia from becoming DKA in patients with pumps. Pumps can experience technical failures, they may “disconnect” from a patient, or the tubing can fail – all of which can lead to hyperglycemia. Once any acute issues are dealt with, the pump itself can be evaluated/repaired/replaced. To avoid any confusion, Dr. Lieb recommends selecting a new infusion site as well, if possible.

Insulin Pumps in the Hospital

Most patients do fine in the hospital with their own insulin pumps. It is important to make sure a patient who plans to use their own pump during a hospitalization, is awake enough and not too sick to manage their pump. Dr. Lieb mentions that for many patients, the insulin pump provides patients with some degree of control and autonomy that can be very reassuring and help fortify the therapeutic relationship. Thus, if possible, it may be beneficial to empower a patient to manage their blood sugar with their pump if they are able.

Continuous Glucose Monitors (CGMs)

Like insulin pumps, these are becoming more and more common. They are (supposed to be) calibrated regularly with fingerstick checks and allow for far fewer “pokes.” The use of CGMs in the hospital is a new frontier as there are still questions about accuracy and safety. Dr. Lieb suggests that the potential for these monitors is very exciting, especially in their ability to alarm patients regarding significant changes in blood sugar / serve as an early warning indicator of blood glucose derangements. However, right now, a CGM should not be used entirely in lieu of hospital-grade fingerstick glucometers.

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