Diabetic Ketoacidosis for the OB/GYN

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What is DKA?

  • Diabetic ketoacidosis is a metabolic derangement affecting primarily patients with type 1 diabetes mellitus:

    • Typically in response to some sort of stress, an insulin deficiency is encountered

      • Because of the insulin deficiency, glucose cannot be taken up and metabolized → hyperglycemia.

      • Starvation hormone pathways activate, increasing lipolysis in the liver → free fatty acids → ketosis and acidosis.

      • The liver also doesn’t have insulin to effect uptake of excess glucose, and actually begins a process of proteolysis and gluconeogenesis → worsening ketosis and hyperglycemia. 

      • The hyperglycemia will lead to glucosuria (loss of glucose via the urine), and will cause a further loss of free water and electrolytes → ultimately progressing to impaired renal function. 

  • DKA may also occur in a patient with type 2 diabetes, where a severe relative insulin deficiency precipitates DKA or a related condition known as hyperosmolar hyperglycemic state (HHS). 

Diagnosis of DKA

  • T1DM with a precipitating event that may cause metabolic derangement and difficulty with giving insulin therapy:

    • Infections or other acute major illness

    • A new diagnosis of T1DM

    • Non-use (accidental or purposeful) of prescribed insulin therapy

    • Use of drugs which may affect carbohydrate metabolism: steroids, terbutaline, 2nd generation atypical antipsychotic agents

    • Cocaine use

    • Malfunction of insulin pumps - less common with newer systems, but still an important contributor!

  • Presentation is usually rapid onset, <24 hours:

    • Neurologic changes - confusion, stupor, coma, seizures

    • Abdominal pain - nausea, vomiting

    • Signs of volume depletion - tachycardia, dry mucous membranes, hypotension

    • “Fruity odor” due to exhaled acetone

    • “Kussmaul respirations” in severely affected patients - compensatory hyperventilation 

  • Laboratory evaluation:

    • CBC

    • BMP, with anion gap calculation

      • DKA with the production of ketones will produce an anion-gap metabolic acidosis (more on that momentarily)

      • Pseudohyponatremia is often present: correct the Na value (Na concentration falls by 2 mEq/L for each 100 mg/mL increase in glucose)

      • Potassium: will often be normal on serum values, but DKA represents a state of significant relative potassium deficit due to urinary losses and shifting of potassium extracellularly with insulin deficiency

        • When insulin is replaced, potassium is driven back into cells and will lower serum potassium - so must be replaced alongside insulin therapy! 

    • UA/ketones

    • Serum ketones / beta hydroxybutyrate 

    • Urine and serum osmolality

    • ABG - especially if serum bicarbonate is very low, or hypoxia is noted

      • On a VBG or ABG - you’ll see low pH with low bicarbonate value → metabolic acidosis

        • Remember in pregnancy, bicarbonate is typically a little lower due to compensation for chronic respiratory alkalosis -- so be sure to look at that value closely! 

    • Investigation of underlying cause -- ie., cultures/imaging if infection suspected; A1c to assess control over time; amylase/lipase if pancreatitis suspected

Treatment of DKA

Important: most large institutions will have a DKA protocol! Check your institution’s policies/procedures and note that in some places, ICU admission will be required for various levels of DKA. We present some pearls here:

Two primary things to do:

  • 1) Correction of fluid and electrolyte abnormalities

    • Give isotonic fluid (LR or NS) to replete extracellular volume losses and stabilize cardiovascular status.

      • If in shock, will need rapid bolusing.

      • If hypovolemic but not in shock, often start with 15-20 ml/kg lean body weight per hour for a few hours, before slowing down. 

      • If euvolemic, slower fluid infusion as clinically indicated. 

        • Most protocols will call for NS as the primary fluid -- however, the chloride load of NS may actually worsen acidosis initially! 

          • Two RCTs (only one mentioned in the podcast) have been performed in adults comparing LR to NS -- finding LR had a mild trend towards faster improvement, but there were no major differences otherwise. 

          • We bring this up as that trend towards faster improvement of acidosis in pregnancy may be of particular consideration - a faster improvement of pH may improve fetal appearance on monitoring. 

    • Fluid choice is often dictated by electrolyte concentrations:

    • Potassium should also be administered as the deficit will often be present:

      • If K < 3.3, KCl should be given at 20-40 mEq/hr, often added to the saline

      • If K 3.3 - 5.3, KCl 20-30 mEq is added to each liter of fluid ongoing

      • If K > 5.3, potassium does not need to be repleted (yet). 

        • Frequent monitoring of K is required, and may often in the initial stages need to be checked on an hourly basis.  

    • Other electrolytes can be in deficit, particularly phosphate and bicarbonate. However, these should not be directly repleted in most circumstances, with the exception of the most critically ill patients. 

  • 2) Administer insulin

    • IV insulin should be given for all patients alongside potassium repletion as we already described.

      • Remember - K may look normal on the BMP, but often is in deficit!

    • Short acting insulins (aspart, lispro, or regular) are preferred at the outset; long-acting insulins should be held until patient is more stable.

      • In mod-severe disease, often start with IV bolus of regular insulin at 0.1 u/kg, followed within five minutes by an infusion of 0.1u/kg/hr. 

        • Again -- most institutions have protocols that will calculate this out for you and prevent errors in administration! 

        • The effect of these doses are to bring serum glucose down 50-70 mg/dL per hour, which is usually about as fast as it can go!

        • Once glucose is around 200 mg/dL, insulin infusion should decrease to 0.02-0.05 u/kg/hr and fluids for repletion should switch to a dextrose-containing product. 

          • If glucose falls too rapidly below 200 mg/dL, can precipitate cerebral edema/injury. 

    • Once a patient is only in mild DKA or transitioning out of it, can add longer-acting agents back.

Other considerations for pregnancy:

  • Symptoms and treatment for pregnant folks are not different!

  • DKA is unfortunately more common in pregnancy, as: 

    • insulin requirements increase rapidly, predisposing patients more often to potential deficiencies

    • There are more opportunities for decompensation: n/v early pregnancy, food aversions, preterm labor, use of steroids for FLM, UTI/pyelonephritis, social concern for “harming baby” with insulin.

  • Recall normal pregnancy physiology is respiratory alkalosis -- so a pH of 7.36 may seem normal for most patients, but can represent significant acidosis in pregnancy!  

  • Consider LR for resuscitation of the pregnant patient: potentially faster improvement of pH in the first hour of treatment due to less chloride load. 

  • Consider tighter targets for glucose control with DKA (getting to 100-150 mg/dL, rather than 200, counterbalancing this with risk of cerebral edema from overcorrection). 

  • During acute DKA - fetal status is often not reassuring! 

    • If mom’s pH is 6.9, baby’s is the same or worse -- manifests with absent variability, decelerations.

    • May take several hours to resolve 

    • DKA alone is not an indication for delivery!

      • It’s preferred to try to resolve the metabolic derangements before proceeding with delivery - better maternal and fetal outcomes with waiting than proceeding with delivery with unstable maternal condition.