Diabetic ketoacidosis: Clinical sciences

Last updated: June 26, 2024

Diabetic ketoacidosis: Clinical sciences

Endocrine Midterm

Endocrine Midterm

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Sheehan syndrome
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Anatomy of the thyroid and parathyroid glands
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Diabetic ketoacidosis: Clinical sciences
Diabetes mellitus (pediatrics): Clinical sciences
Diabetes in pregnancy (GDM, T1DM, and T2DM): Clinical sciences
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Diabetes mellitus (Type 2): Clinical sciences
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Decision-Making Tree

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Diabetic ketoacidosis, or DKA for short, is a life-threatening complication of diabetes mellitus characterized by a severe insulin deficiency and glucagon excess. It typically but not exclusively occurs in the setting of type 1 diabetes, with common triggers that include illness or infection, as well as known diabetes with suboptimal glycemic control or interruption in therapy.

The diagnosis of DKA relies primarily on blood work showing metabolic acidosis and hyperglycemia, as well as ketones in the urine.

Now, if you suspect DKA, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.

DKA generally presents as unstable, so stabilize the airway, breathing, and circulation. Next, obtain IV access, and give a 1-liter bolus of isotonic IV fluid.

Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and provide supplemental oxygen, if needed.

Once you stabilize the patient, obtain a focused history and physical exam. History often reveals polyuria, polydipsia, and unintentional weight loss, as well as nausea, vomiting, and diffuse abdominal pain. These are commonly associated with a recent precipitating factor like illness or infection. Additionally, there might be a known history of diabetes with inadequate glycemic control or recent disruption in therapy.

On the other hand, physical exam might reveal a confused, somnolent patient with tachycardia, hypotension, and dry mucous membranes. Also, you might see a pattern of deep, rapid breathing known as Kussmaul respirations, and a fruity odor to the breath.

Based on these findings, suspect DKA. Next, order labs, including an ABG or VBG, CMP, and serum and urine ketones like beta-hydroxybutyrate.

Next, review the lab results and assess diagnostic criteria for DKA, which include a blood glucose above 250 milligrams per deciliter, a pH below 7.3, and a serum bicarbonate level less than 15 milliequivalents per liter, indicating a metabolic acidosis. Additional criteria includes an elevated anion gap, and elevated serum and urine ketones.

If the DKA criteria are not met, you should consider alternative diagnoses. On the other hand, if the lab results show that DKA criteria are met, you can diagnose DKA and begin insulin treatment.

Here’s a clinical pearl to keep in mind! There are several conditions that can mimic DKA. Hyperosmolar hyperglycemic state, or HHS for short, is most commonly seen in type 2 diabetes and presents with hyperglycemia, with blood glucose over 600 mg/dL, as well as hyperosmolarity. But here’s the big difference; unlike DKA, in HHS there is no acidosis.

On the flip side, like DKA, other conditions like starvation and alcoholic ketoacidosis can cause ketoacidosis, and in both of these conditions, blood glucose can be elevated, but it’s rarely over 200 mg/dL. Ok, now that we’ve diagnosed DKA, let’s turn our attention to management.

Start IV fluids, as well as a bolus of IV insulin, dosed at 0.1 unit per kilogram, followed by a constant IV insulin infusion at 0.1 units per kilogram per hour. At the same time, pay attention to the serum potassium level, because insulin and fluid resuscitation can lower serum potassium levels.

If the serum potassium is above reference range, no potassium replacement is needed. On the other hand, if the serum potassium is below reference range or even within reference range, add potassium to the IV fluids. In fact, if the potassium is below the reference range, it's actually necessary to replace potassium before even starting insulin!

Here’s a high-yield fact to keep in mind! In DKA, the acidosis causes potassium to leave the cells and enter the bloodstream. However, as soon as you give insulin, that potassium is going right back in the cells, dangerously decreasing its blood levels. So a modestly low potassium of 3 could quickly reach a lethal level of 2.5 if you start the insulin drip before appropriately replacing the potassium.

And now, a clinical pearl! Order a CMP every 2 to 4 hours to identify electrolyte imbalance, hold insulin infusion if potassium is low, and initiate replacement as appropriate. But remember, DKA patients often have renal dysfunction, so be mindful that they may need more cautious potassium replacement. Once potassium levels are normal, don’t forget to restart insulin.

Sources

  1. "American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update" Endocr Pract (2022)
  2. "Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State" Med Clin North Am (2017)
  3. "Hyperglycemic crises in adult patients with diabetes" Diabetes Care (2009)
  4. "Harrison’s Principles of Internal Medicine, 21st Edition" McGraw Hill Education (2022)
  5. "Utility of plasma beta-hydroxybutyrate to define resolution of diabetic ketoacidosis" Pediatr Diabetes (2022)