How to care for DKA: An Expert Nurse’s Guide to Diabetic Ketoacidosis

Patients who don’t know they are a type 1 diabetic yet

Patients who don’t take insulin as prescribed

If there is an infection, most commonly Pneumonia or UTI

Steroids, high-dose thiazide diuretics, dobutamine, terbutaline, second-generation atypical antipsychotics, or SGLT2 inhibitors

Cocaine use has been associated with recurrent DKA

May be from delayed gastric emptying and ileus (where a section of the intestinal wall does not perform peristalsis as normal)

Common in DKA, but almost never happens with HHS

Increased urinating is due to the osmotic diuresis described above, and the increased thirst is due to the hyperosmolality of the blood

This is due to water losses, as well as fat losses from the massive lipolysis that occurs

Lethargy, confusion, and/or obtundation can occur. Focal signs are possible as well. AMS tends to be worse in HHS because these patients often have a higher degree of hyperosmolarity.

Increased respiratory rate

This is termed Kussmaul respirations. This is the body trying to breathe off extra CO2 to compensate for the increased acidity caused by the DKA

Dry Mucous Membranes

Looking in their mouth and at their tongue is a great indicator of hydration status. These patients will be dry as a bone.

Temp: Often normal, but may high if infection

HR: Often tachycardic due to dehydration +/- infection

BP: May be low with severe hypovolemia

SPO2: Usually normal

Respiratory Rate: often >20 rpm (Kussmaul respirations)

Heart: Fast and regular

Lungs: usually clear but frequent and deep

Pulse: Peripheral pulses may feel weak and thready

Abdomen: May have some tenderness but shouldn’t have rebound or guarding

Patients in DKA are prone to severe electrolyte abnormalities such as hypokalemia, which can cause deadly cardiac arrhythmias to occur

Glucose monitors will often read “HI” if above 600 g/dL. However, even “euglycemic” DKA has occurred with near-normal glucose levels.

Any sick patient that may require ICU should have at least 2 IVs placed, preferably at least 20g. These patients will need a large volume of fluid replacement as well as will likely require an insulin drip and IV potassium.

Be sure to draw a gold top for the chemistries, and a lavender top for CBC. If a VBG is ordered, also draw a green top and place it on ice.

These patients are often visibly dehydrated and tachycardic. Hang 1-2L of NS open to gravity (and of course obtain an order to verify). 

Ask for and administer medications such as Zofran or pain meds if the patient is nauseous or in severe pain

This is the level drawn either with a capillary glucose monitor or within the CMP of the labs. Patients in DKA often have blood sugars between 350-550 mg/dL

A high anion gap acidosis is the hallmark of DKA. The AGAP is usually >20 in DKA. This is usually due to the markedly reduced serum bicarb levels, as well as the accumulation of ketone bodies.

This is always elevated in HHS, but not always elevated in DKA. >295 mOsm/kg is considered hyperosmolar, and in HHS often levels exceed 320. Effective serum osmolality can also be calculated here. 

Serum CO2 in the CMP is equivalent to Bicarb in an ABG.

If the CO2 aka Bicarb is lower than 18, this generally indicates metabolic acidosis.

Most patients with DKA are mildly hyponatremic (low sodium), but their levels will often appear even lower. This is because the high blood sugar pulls water out of cells and dilutes the sodium.

For an accurate sodium level, you should add 2 mEq/L for each 100mg increase in glucose above 100 mg/dL. You can also use this calculator.

Most patients with DKA and HHS have a total body deficit of 300-600 mEq of potassium.

This is because a lot of the potassium is urinated out along with water and ketones.

Lab levels usually appear normal and sometimes even elevated – but don’t be fooled!

Due to hyperosmolality and insulin deficiency, intracellular potassium moves out of cells and into the extracellular fluid.

Once insulin is administered, the potassium will be transported back into the cells, and the patient can be left with severely low potassium which can cause arrhythmias and even death.

Kidney function may be elevated from prerenal acute kidney injury from dehydration and hypovolemia. The patient may also have some diabetic nephropathy.

Most patients with DKA will have mild leukocytosis, and this is usually proportional to how many ketones are in the blood. It may also be related to cortisol and stress hormones as well.

A WBC > 25 or bands >10% should raise suspicion of infection.

ABGs are rarely needed in DKA. Remember DKA is metabolic acidosis, and there often is respiratory compensation.

If drawn, this means the pH will be acidic (< 7.35), the HCO3 will be low (<18), and the CO2 will also be low (<35) to compensate.

A VBG is often ordered instead of a full ABG in patients with suspected DKA. We are mainly evaluating the patient’s pH and bicarb levels, which are essentially equivalent to their ABG counterparts.

Serum ketones can be drawn to directly detect ketones within the blood. These do not need to be drawn if the patient has a AGAP acidosis with hyperglycemia, but will depend on the facility and ordering Provider.

Serum acetone or beta-hydroxybutyrate can both be ordered, and different hospitals will have different options.

A urinalysis will often show a decreased specific gravity from the osmotic diuresis. Additionally, it will often show large glucose and often ketones.

Amylase and lipase may be ordered if pancreatitis is suspected, and lipids may also be ordered (but usually with morning labs).

The first step in treating DKA is to replace IV fluids, usually with Normal Saline, which helps stabilize vital signs, replace fluid losses, increase insulin responsiveness, and reduce stress hormone levels.

Remember that severely high blood sugar causes severe dehydration, so these patients usually need a lot of fluid. 

This is usually with 2-4L NS for the first 3-4 hours, infused at 1L per hour. 

If the patient has a history of CHF or advanced renal failure, this should be infused slower with careful monitoring for fluid overload.

As long as potassium >3.3, Insulin can be started.

Each hospital will have their own insulin drip protocol. Often a bolus is given first of 10 units (0.1u/kg body weight). Then the infusion is started at 0.1u/kg/hr. 

Regular and rapid-acting insulins are equally effective at treating DKA and HHS.

Once the serum glucose reaches between 200-300, dextrose is usually added to the IV fluid until the acidosis resolves.

If >5.3 mEq/L: IV Potassium is held off until levels drop below 5.3. These are checked hourly.

If 3.3 – 5.3 mEq/L: IV potassium is started as long as the patient is making >50ml/hr of urine, indicating appropriate renal function. 20-30mEq is usually added to each liter of IV fluid.

The goal is to maintain the potassium between 4 – 5 mEq/L.

If <3.3 mEq/L: The patient requires 20-40mEq/hr until the potassium is above 3.3. This is often added to NSS or ½ NS.

Insulin therapy should not be started until this level is above 3.3!

After the first few hours, IV fluids should be continued at a slower rate. This will be selected by correcting the sodium level for hyperglycemia.

If the sodium level is still low, Normal saline is usually continued.

If the corrected sodium is normal, hypotonic saline is started (i.e. 1/2 NS).

These are usually continued at a rate between 250-300ml/hr.

While it may seem counterintuitive, IV dextrose is added to the IV fluids once the blood sugar reaches somewhere between 200-300 mg/dL.

This is because insulin is still needed to “close the gap” and reverse the acidosis, but the glucose can still drop too much. If the blood glucose drops below 200-300mg/dL can increase the chance of cerebral edema!

In HHS, its best not to let the glucose drop below 250-300 mg/dL, and in DKA no less than 200 mg/dL.

An example of a fluid would be D5 1/2 NS (likely with potassium added as well).

Check out my article on IV FLUIDS!

Each hospital should have a facility protocol when it comes to insulin drips.

Usually, this requires blood glucose checks every hour.

Once the glucose drops below 250 mg/dL, fluid with dextrose is usually started until the AGAP normalizes, otherwise the patient will become hypoglycemic.

Lowering the glucose too much in these patients can lead to cerebral edema.

As discussed above, this should be monitored frequently.

A BMP is usually checked every 2-4 hours while on an insulin drip.

Monitor for tachycardia, ectopy, or any arrhythmias.

Severe hypokalemia and acidosis can lead to fatal arrhythmias like VFIB, Asystole, and PEA.

Significant acidosis and hypovolemia can cause hypotension.

When the body is acidotic, medications like vasopressors don’t work as well as they should.

Once the AGAP returns to normal, the gap is considered ‘closed” and the patient does not require an IV insulin drip anymore.

They are usually transitioned to subcutaneous insulin at this time.