Yes, you can be in diabetic ketoacidosis with a normal or near-normal blood sugar. The condition is called euglycemic DKA, and it’s defined by blood glucose under 250 mg/dL alongside the same dangerous acid buildup that happens in classic DKA. Because most people associate DKA with sky-high blood sugar, the normal-range reading can mask a serious emergency.
What Euglycemic DKA Looks Like
In classic DKA, blood sugar often climbs above 300 or even 500 mg/dL. That spike is one of the first red flags. Euglycemic DKA produces the same metabolic crisis, with blood that becomes dangerously acidic and high levels of ketones, but glucose stays below 250 mg/dL. In some cases it sits well within a range most people would consider “normal.”
The formal criteria are the same as regular DKA in every way except the glucose number: blood pH drops below 7.3 (normal is around 7.4), bicarbonate falls below 18 mEq/L, and ketones are elevated in the blood. Those changes mean your body is breaking down fat at a rate it can’t safely handle, flooding the bloodstream with acidic byproducts. The only difference is that your glucose meter won’t warn you.
Why Blood Sugar Stays Low
The core problem in euglycemic DKA is a carbohydrate deficit rather than a pure insulin shortage. When your body runs low on available carbohydrates, whether from fasting, vomiting, a low-carb diet, or a medication that flushes glucose out through the kidneys, it shifts to burning fat for fuel. That fat breakdown produces ketone bodies. Normally, a small amount of insulin would keep this process in check. But if insulin levels are even mildly insufficient while carbohydrate stores are depleted, the balance tips toward runaway ketone production.
At the same time, the hormone glucagon rises relative to insulin. That elevated glucagon-to-insulin ratio drives the liver to oxidize more fat and churn out more ketones. In classic DKA, the same hormonal shift also causes the liver to dump large amounts of glucose into the blood. In euglycemic DKA, that glucose-producing pathway is less active, or the glucose is being cleared faster than it’s produced, so blood sugar doesn’t spike the way you’d expect.
Common Triggers
A class of type 2 diabetes medications called SGLT2 inhibitors is one of the most recognized triggers. These drugs lower blood sugar by blocking the kidneys from reabsorbing glucose, so excess glucose leaves through urine. That constant glucose drain can keep blood sugar looking reassuringly normal even while the body is starving for carbohydrate energy at the cellular level and ramping up ketone production. Common SGLT2 inhibitors include canagliflozin, dapagliflozin, and empagliflozin.
Other situations that can set off euglycemic DKA include:
- Reduced food intake. Illness, surgery recovery, nausea, or intentional fasting can create the carbohydrate deficit that starts the cascade.
- Pregnancy. The metabolic demands of pregnancy increase ketone production and can push someone with diabetes into ketoacidosis without a dramatic glucose rise.
- Heavy alcohol use. Alcohol suppresses the liver’s ability to produce glucose while simultaneously promoting ketone formation.
- Insulin pump failure. A partial delivery problem may provide just enough insulin to keep sugar in range but not enough to fully suppress ketogenesis.
The condition affects both type 1 and type 2 diabetes. People with type 1 are already prone to DKA because they produce little or no insulin. People with type 2 are most commonly affected when SGLT2 inhibitors are combined with one of the triggers above, like an acute illness or reduced eating.
Symptoms to Watch For
Because glucose readings look fine, the warning signs you need to pay attention to are the ones caused by acid and ketone buildup rather than high sugar. Nausea, vomiting, and abdominal pain are common early signs. You may feel unusually fatigued, confused, or short of breath. Rapid or deep breathing is the body’s attempt to blow off excess acid through the lungs. A fruity smell on the breath, caused by acetone (a type of ketone), is another clue.
The danger is that without the classic “high sugar” alarm, people often attribute these symptoms to a stomach bug or general fatigue and delay seeking help. If you have diabetes and you’re feeling sick with any combination of these symptoms, checking ketones is more informative than checking glucose alone.
Why Blood Ketone Testing Matters
A standard finger-stick glucose reading will not catch euglycemic DKA. Ketone testing is the key diagnostic step. You can test ketones with urine strips or a blood ketone meter, but the two aren’t equally reliable. Blood ketone meters measure beta-hydroxybutyrate, the primary ketone your body produces during DKA. Urine strips detect a different ketone (acetoacetate) and reflect what your body was doing hours earlier rather than right now.
Research comparing the two methods found that blood ketone testing was associated with fewer hospitalizations, faster recovery from DKA episodes, and lower healthcare costs. If you take an SGLT2 inhibitor or have type 1 diabetes, keeping a blood ketone meter at home gives you a direct, real-time reading when symptoms feel off, even if your glucose looks perfectly normal.
Preventing Euglycemic DKA on SGLT2 Inhibitors
The simplest prevention rule: stop the medication when your body is under stress. The American Diabetes Association recommends pausing most SGLT2 inhibitors three days before any scheduled surgery (four days for ertugliflozin). For unplanned situations, the same logic applies in a less tidy way. If you’re unable to eat or drink normally, are vomiting, are dehydrated, or have an acute illness, pausing the medication removes the main driver of continued glucose dumping.
The mnemonic some hospitals use is SSTOP: Stop SGLT2 inhibitors Three days before Procedures. But the principle extends beyond surgery. Any scenario where oral intake drops significantly is a reason to pause. You should only restart once you’re eating and drinking normally again.
How Treatment Differs From Classic DKA
Treating euglycemic DKA follows the same broad approach as regular DKA: fluids and insulin to shut down ketone production. The key difference is that because blood sugar is already low or normal, giving insulin without also giving sugar could cause dangerous hypoglycemia. So treatment typically includes a dextrose (sugar) infusion running alongside insulin from the start, rather than waiting until glucose drops below a threshold as in classic DKA. This lets clinicians deliver enough insulin to stop the ketone storm without crashing blood sugar in the process.
Recovery timelines are similar to standard DKA. Most people see acid levels normalize within 12 to 24 hours with appropriate treatment. The episode itself is just as dangerous as classic DKA if it goes unrecognized, which is exactly why awareness of the condition matters so much.