Diabetic Ketoacidosis for the OB/GYN
/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.