Setting: emergency department (ED)
CC: “He is confused and breathing fast.”
VS: R: 34 breaths/minute; BP: 106/68 mm Hg; P: 122 beats/minute; T: 99.8°F
HPI: A 34-year-old man with a history of type 1 diabetes is brought to the ED by his family for confusion and lethargy for the last day. The patient has been a lifelong diabetic who also has some unclear psychiatric issues. The family says he stopped taking his insulin a few days ago for unclear reasons—he may have just run out of his medications.
PE:
General: lethargic, disoriented, rolling around in bed, respiratory distress
Chest: clear to auscultation
Abdomen: soft, nontender
Cardiovascular: no murmur, no gallop
Neurological: unable to determine whether there are focal deficits
Initial Orders:
CHEM-7
Normal saline (NS) bolus
Arterial blood gas (ABG)
UA
Acetone, beta-hydroxybutyrate levels
Electrocardiogram (ECG)
What is the single most important test in diabetic ketoacidosis (DKA)?
a. Glucose level
b. pH
c. Ketone and/or acetone levels
d. Serum osmolarity
Answer b. pH
The glucose level is not as important as knowing if the patient is acidotic. Glucose levels can fluctuate wildly from high to medium, but if the patient’s pH on an ABG or serum bicarbonate on chemistry is near normal, it does not matter. The same is true of ketones, acetone, beta-hydroxybutyrate, or acetoacetate. The level of these ketone bodies is not as important as the level of accumulated acid.
Glucose, ketones, and osmolarity are not as important as pH and bicarbonate levels.
Move the clock forward the absolute minimum amount of time needed to get results of the ABG. Recheck vital signs and consult the intensive care unit if it has not already been done. Re-bolus with intravenous (IV) fluids. Use NS or Ringer lactate. More than half the problem in DKA is inadequate amounts of fluid.
Laboratory Test Results:
CHEM-7:
Glucose 725 mg/dL
Bicarbonate 12 mEq/L
Chloride 100 mEq/L
K 6.4 mEq/L
Sodium 126 mEq/L
ABG: pH 7.12; partial pressure of carbon dioxide (PCO2) 28 mm Hg; partial pressure of oxygen (PO2) 95 mm Hg
UA: glucose 1000 mg/dL; ketones +++
Acetone, beta-hydroxybutyrate levels: markedly elevated
ECG: sinus tachycardia, normal T wave, no ST abnormalities
Glucose 100 Up = Sodium 1.6 Down
For every 100 mg/dL above normal glucose level, sodium level is decreased by 1.6 mEq/L.
What is the mechanism of the artificial decrease in sodium?
a. It is a laboratory artifact.
b. Acid interferes with sodium measurement.
c. Hyperglycemia pulls water out of cells, diluting out the sodium.
d. Ketone bodies bind sodium, removing it from circulation.
Answer c. Hyperglycemia pulls water out of cells, diluting out the sodium.
Knowing the numerical relationship between sodium and glucose is indispensable to accurately assessing the anion gap. In addition, because hyponatremia causes confusion and hyperglycemia causes confusion, it is important to be able to address and correct the proper abnormality. When glucose levels markedly increase, it pulls water out of cells. Because the total number of sodium molecules do not change, the extra water in the vascular space drives the sodium level down.
Insulin uses a tyrosine kinase receptor.
Acid stimulates hyperventilation at the brainstem.
What is the mechanism of hyperkalemia?
a. Transcellular shift (exchange) for acid (H+)
b. Failure of renal excretion
c. Cell lysis
d. Potassium bound by ketone bodies
Answer a. Transcellular shift (exchange) for acid (H+)
When acid or hydrogen ions (H+) build up in the blood, the majority of live cells in the body buffer the acid by absorbing it. To maintain electrical neutrality, the cells will release a K+ for each H+ it picks up. In addition, insulin drives potassium into cells with glucose. If there is no insulin, the cells will not receive potassium. Also, insulin has a direct stimulatory effect on sodium-potassium adenosine triphosphatase (Na+/K+-ATPase). Without insulin, the cells will not pick up insulin by stimulation of Na+/K+-ATPase.
Did you know insulin stimulate Na+/K+-ATPase to drive K+ into cells?
Two liters of NS were given in the first hour. A meaningful fluid bolus is 20 mL/kg. Repeat the chemistry level every 1 to 2 hours to guide fluid and insulin dosing and to determine the need for IV bicarbonate. It is not precisely clear when IV bicarbonate is needed, but for most cases, when the pH is <7.2, it is acceptable to use.
Orders:
IV insulin continuous drip
NS bolus
CHEM-7
Venous blood gas
Move the patient to the intensive care unit (ICU) if not done
Hyperkalemia is expected in all patient’s with metabolic acidosis with an increased anion gap.
Why is the K+ level increased?
There is a transcellular shift with H+.
There is no insulin to drive Na+/K+-ATPase.
What is the difference between venous pH and arterial pH?
a. Venous < Arterial
b. Arterial > Venous
c. Equal
Answer c. Equal
If there is no respiratory disease, arterial and venous pH should be essentially equal. A difference of a few hundredths of a point is clinically irrelevant. This is why you can use venous blood gasses (VBGs) to monitor DKA response to management. There is no reason to torture patients with the pain of an arterial puncture for no reason when you can do a venous puncture.
Use venous blood gasses to monitor DKA response to therapy.
Move the clock forward every 15 to 30 minutes for the first hour or two. Use “Interval History” to see if there is a clinical response to the use of fluids and insulin. There should be a measurable effect within 30 minutes to IV insulin and massive volume replacement. If there is no improvement, repeat the “bolus NS” and “IV insulin” orders.
Orders:
VBG
CHEM-7
NS bolus
IV insulin
What is the mechanism of lethargy and confusion in DKA?
a. Acid inhibits neural transmission.
b. Hyponatremia is the mechanism.
c. Hyperosmolarity dehydrates brain cells.
d. Hyperkalemia interferes with neural transmission.
Answer c. Hyperosmolarity dehydrates brain cells.
Serum osmolarity is usually dependent entirely on serum sodium content. In severe hyperglycemia, the extremely high glucose level acts as an osmotic draw on brain cells. This dehydrates them, and central nervous system (CNS) neural function, especially for cognitive purposes, is worse when dehydrated.
Serum Osmolarity = (2 × Serum Sodium [mEq/L]) + (Glucose [mg/dL]/18) + (BUN [g/dL]/2.8)
The brain does not think well with high osmolarity sucking out the water.
The brain switches to using ketones for fuel.
After 2 hours, the patient’s lethargy resolves, and normal mentation returns. The repeat laboratory test results are:
Glucose 245 mg/dL
K 4.8 mEq/L
Serum bicarbonate 18 mEq/L
pH 7.32
What is the biggest change you must make in management?
a. Stop IV insulin; switch to subcutaneous delivery.
b. Switch to oral fluids.
c. Add potassium to fluids.
d. Move the patient out of ICU.
Answer c. Add potassium to fluids.
As the potassium starts to drop into the normal range, add potassium replacement. This is because the body becomes massively depleted of potassium because of the metabolic acidosis. Acidosis takes potassium out of cells. High blood potassium is excreted at the kidney to protect the heart from fatal arrhythmia. When acidosis corrects, potassium shifts back into cells and blood levels will drop belownormal.
During acidosis, potassium is excreted from kidneys.
The body becomes massively depleted of potassium during metabolic acidosis.
Potassium is added to routine IV fluids. Repeat the VBG every 2 hours until the pH nears the normal 7.4.
You do not have to wait for the ketones to disappear to transfer the patient out of the ICU. The ketone bodies are like garbage that needs time to clear away.
When serum bicarbonate level rises above 20 to 22 mEq/L and pH is above 7.35, you can transfer the patient out of the ICU.
When cells cannot take up glucose because of a lack of insulin, they switch to lipids and free fatty acids as an alternate fuel source. Free fatty acids, unfortunately, come with a toxic end product called ketones. This is why:
• No insulin ensures no glucose uptake.
• Cells eat fatty acids and make ketones.
• Ketones create acid.
Ketones are acid end products of lipid metabolism.