In this episode I will be discussing all about the management of Diabetic Ketoacidosis (DKA) in the ICU patient . I will discuss in detail about the pathophysiology of DKA, patient presentation, signs and symptoms, labs, treatment, monitoring, resolution of DKA and potential pitfalls.
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The Right Pill Pharmacy Podcast
Episode 1 (DKA)
Background
DKA is diabetic ketoacidosis, and happens when your body breaks down fat into fatty acids which the body uses as an alternate source of energy. Remember, in DKA there is either a relative or absolute insulin deficiency occurring. therefore your body cannot utilize the glucose that is in the blood since there is no insulin to transport the glucose into cells where it will be used as energy in the form of ATP. Unfortunately the byproduct of fatty acid metabolism is ketones which are acidic in nature. This is where the ketoacidosis comes from in DKA. Anyway, DKA can be life threatening if left untreated. DKA is a complications of uncontrolled diabetes. It most often occurs in type 1 diabetics, although it can occur in type 2 diabetes under conditions of extreme stress such as trauma or infection. DKA is usually precipitated by some triggering event such as stress and infection, however based on my experience on ICU rounds, the most common trigger for dka is due to medication non- compliance.
Patient presentation
A typical dka pt will present with a blood glucose below 800 mg/dl usually in the range of 350 to 500 mg/ dl. Common S&S include nausea, vomiting, polyuria, polydipsia, abdominal pain, altered mental status, and dehydration. More severe symptoms include, tachypnea, metabolic acidosis, hypotension/shock, cerebral edema, pulmonary edema, respiratory failure, seizures, coma, and death. Obviously, dka is a medical emergency and needs to be treated in a timely manner.
Treatment
Successful treatment of dka consist of
- 1. IV fluid replacement
- 2. Replacement of electrolytes
- 3. Correction of hyperglycemia
- 4. Correction of metabolic acidosis
IV fluid replacement
Pts with Dka typically present with severe dehydration. This is because the glucose levels are so high in the blood that it causes you to urinate excessively hence the polyuria, which in turn leads to increase thirst hence the polydipsia. In fact, the dehydration can be so severe that pts can develop hypovolemic shock, requiring these pts to be admitted to the ICU and placed on vasopressors. It is for this reason that dka pts require about 1 liter/hr of isotonic fluids (NS ) in order to correct the intravascular depletion. Once the intravascular depletion has been corrected you can change the IV fluids to 1/2 NS if the corrected sodium is normal or high, otherwise continue to give NS if the corrected sodium is low. The reason why we use the corrected sodium, is because in dka, the water shifts from inside the cells to outside the cells in order to dilute the glucose in the blood. This fluid shift will also dilute the sodium causing hyponatremia. The pt will experience the effects of hyponatremia even though the total body stores of sodium are unchanged.
Replacement of electrolytes
Dka pts often present with electrolyte disturbances. Potassium, sodium, magnesium, and phosphorus levels can all be altered mostly due to fluid shifts from the intracellular space to the extra cellular space, excessive diuresis, and excessive vomiting. All these factors will ultimately cause a slew of electrolyte abnormalities. Potassium replacement in a dka pt is especially critical because of its effect on the heart such as arrhythmias. It is important to realize that before you correct the hyperglycemia in dka with insulin, you must make sure that the potassium levels are >/= 3.3 meq/L. If potassium levels are < 3.3 meq/L you need to hold the insulin. The reason for this is because when you give insulin it will drive the potassium into cells further decreasing potassium levels. This in turn can lead to potentially life threatening arrhythmias.
Potassium supplementation can be done at a rate of 20 to 40 meq/hr until potassium levels are above 3.3 meq/L. This is provided that a central line is in place.
Magnesium levels should also be checked and supplemented as necessary. Remember, if magnesium is not corrected you will never be able to adequately correct Potassium levels.
Phosphorus levels will inevitably decrease. The reason for this is because as the glucose moves from outside the cells to inside the cells via insulin, the cells can now utilize glucose for energy in the form of ATP. Therefore phosphorus levels will decrease and therefore will need to be supplemented. This is particularly important if the dka pt end up on a ventilator due to respiratory failure. If phosphorous levels are below 1 mg/dl then the diaphragm will become weak, and the pt will have difficulty coming off of the ventilator.
Correction of hyperglycemia
Once both the fluid deficit and potassium deficit has been corrected then at this time you can begin correcting the hyperglycemia. This is an important point to remember because if you give insulin before correcting the fluid deficit, then this can lead to a worsening of the pts overall hemodynamics ultimately causing a fatal outcome. Regular Insulin can be given as a bolus of 0.1 units/kg, followed by a continuous infusion of
0.1 units/kg/hr. If you choose not to give a bolus then start the infusion at
0.14 units/kg/hr. The blood glucose levels should be decreasing by about 50-70 mg/dl per hour. It is important that you don’t correct the blood glucose faster than this rate, because it can potentially cause cerebral edema. If the blood glucose doesn’t decrease by this amount then you need to double the rate of insulin infusion. Once the blood glucose reaches 200 mg/ dl then you can decrease the rate of insulin infusion to 0.02 - 0.05 units/kg/hr. At this point you can also add dextrose to the saline solution. Adding dextrose to the IV fluids will ensure that the pt doesn’t become hypoglycemic, which is a common pitfall when treating dka pts with insulin.
Correction of metabolic acidosis
Metabolic acidosis is one of the major findings in a dka pt. The acidosis that occurs in dka is due to the metabolism of free fatty acids resulting in the formation of ketones, especially beta-hydroxybutyrate. The administration of insulin reverses this process thus correcting underlying cause of the metabolic acidosis. Insulin administration is therefore the definitive treatment for the metabolic acidosis that occurs in dka. Sodium bicarbonate administration is controversial, and doesn’t offer any benefit. If anything it can be harmful to the pt. If you do decide to administer sodium bicarbonate it should be done when the arterial pH is < or = to 6.9. In this case you can dilute 100 meq of sodium bicarb in 400 ml of sterile water with 20 meq of kcl and infuse at 200 ml/hr. The serum bicarb levels should be repeated every 2 hours until the pH is > or = to 7.0.
Resolution of dka
The resolution of dka becomes evident when the following happens:
The venous pH is > than to 7.3
The serum bicarbonate is > than 14
The AG is < than 12
The pt is eating
Serum beta-hydroxybutyrate is within normal limits.
Glucose should be less than 200 mg/dl
Once dka resolves, then at that point the pt may be transitioned to subcutaneous insulin. Keep in mind that the insulin infusion should continue for 2 hours after the first dose of subcutaneous insulin. This ensures that the subcutaneous insulin has adequate time to take effect before stopping the insulin infusion. Otherwise the pt can go back into dka. This is a major pitfall that I have seen happen while on ICU rounds, so don’t make that mistake. As far as re-starting subcutaneous insulin, if the pt had a home regimen that they were on prior to hospitalization then you can just re-start that home regimen. If the pt is insulin naive then you can administer anywhere from 0.5 - 0.8 units/kg per day, and divide this 50/50 into a basal/bolus regimen assuming the pt is eating.
Monitoring
Monitoring of a dka involves
1. Hourly monitoring of blood glucose until stable
2. BMP ( K, MG, Phos, NA,) and venous pH every 2-4 hours
3. Serum beta hydroxybutyrate levels
4. AG closure
5. BUN/ serum creatinine every 2-4 hours
6. Serum bicarb levels

