Diabetic Ketoacidosis: Symptoms, Causes & Emergency Treatment

What Is Diabetic Ketoacidosis?

Diabetic ketoacidosis (DKA) is a severe metabolic complication of diabetes characterized by high blood sugar, elevated ketone levels, and metabolic acidosis. It occurs when insulin deficiency causes the body to break down fat for energy, producing toxic ketone acids. DKA is most common in type 1 diabetes and requires emergency hospital treatment.

Diabetic ketoacidosis represents one of the most serious acute complications of diabetes mellitus. The condition develops when there is an absolute or relative deficiency of insulin in the body, preventing cells from using glucose (blood sugar) as their primary energy source. When this happens, the body enters a state of metabolic crisis, shifting to fat breakdown as an alternative energy pathway.

The term "ketoacidosis" combines two key aspects of the condition: "keto" refers to ketones, which are acidic byproducts of fat metabolism, and "acidosis" describes the dangerous lowering of blood pH that occurs when these ketones accumulate. Under normal circumstances, the liver produces small amounts of ketones during fasting or prolonged exercise, but in DKA, ketone production spirals out of control, overwhelming the body's ability to maintain normal acid-base balance.

Understanding the pathophysiology of DKA is essential for recognizing its seriousness. Without insulin, glucose cannot enter most cells despite being abundant in the bloodstream. The brain sends hunger signals because cells are starving for energy, while simultaneously blood glucose levels climb dangerously high. This creates a paradox where the body is literally swimming in fuel it cannot use. In response, stress hormones like glucagon, cortisol, and adrenaline surge, further worsening the metabolic derangement.

The breakdown of fat tissue releases fatty acids into the bloodstream, which travel to the liver and are converted into ketone bodies: acetoacetate, beta-hydroxybutyrate, and acetone. While ketones can provide some energy to certain tissues, their rapid accumulation acidifies the blood, disrupting vital enzymatic processes and potentially leading to coma and death. The acetone component is volatile and can be detected on the breath as a characteristic fruity or nail polish remover-like odor.

Who Is at Risk for DKA?

While diabetic ketoacidosis most commonly occurs in people with type 1 diabetes, it can also develop in those with type 2 diabetes under certain circumstances. People with type 1 diabetes have an absolute insulin deficiency because their immune system has destroyed the insulin-producing beta cells in the pancreas. Without external insulin administration, they are at constant risk of developing DKA.

In type 2 diabetes, DKA typically occurs during severe physiological stress such as major illness, surgery, or when certain medications like SGLT2 inhibitors are used. A particularly concerning phenomenon called "euglycemic DKA" can occur with SGLT2 inhibitors, where ketoacidosis develops despite relatively normal blood glucose levels, making diagnosis more challenging.

What Are the Symptoms of Diabetic Ketoacidosis?

The symptoms of diabetic ketoacidosis include excessive thirst, frequent urination, nausea and vomiting, abdominal pain, fruity-smelling breath (acetone odor), rapid deep breathing (Kussmaul respiration), confusion, fatigue, and in severe cases, loss of consciousness. Symptoms can develop over hours to days and worsen as ketone levels rise.

The clinical presentation of diabetic ketoacidosis typically follows a progression from early warning signs to more severe manifestations. Recognizing the early symptoms provides a critical window for intervention before the condition becomes life-threatening. The symptoms reflect the underlying metabolic derangements: hyperglycemia causes osmotic diuresis leading to dehydration, while ketone accumulation produces characteristic signs of acidosis.

In the initial stages, symptoms often resemble those of poorly controlled diabetes or simple hyperglycemia. Excessive thirst (polydipsia) and frequent urination (polyuria) occur because the kidneys attempt to excrete the excess glucose, pulling water along with it. This creates a vicious cycle of dehydration that worsens the hyperglycemia by concentrating the blood. Many patients report drinking large quantities of fluid without relief of their thirst.

As ketone production increases and acidosis develops, the body attempts to compensate by increasing ventilation to expel carbon dioxide, a respiratory acid. This produces the classic "Kussmaul breathing" pattern – rapid, deep respirations that may look like the person is trying to catch their breath. The breath often carries the distinctive sweet, fruity odor of acetone, sometimes compared to nail polish remover or overripe fruit. This smell is highly specific for DKA and should prompt immediate medical evaluation.

Gastrointestinal symptoms are common and can be severe, leading to misdiagnosis as viral gastroenteritis or food poisoning. Nausea, vomiting, and diffuse abdominal pain affect the majority of patients with DKA. The abdominal pain can be intense enough to mimic surgical emergencies like appendicitis, and the vomiting further worsens dehydration and electrolyte imbalances. Children and adolescents presenting with severe vomiting should always have their blood glucose checked.

Neurological Symptoms

As DKA progresses, neurological function becomes increasingly impaired. Initially, patients may experience difficulty concentrating, mental sluggishness, and mild confusion. These symptoms can rapidly progress to severe lethargy, obtundation, and eventually coma. The exact mechanism of neurological impairment involves multiple factors including acidosis effects on brain function, dehydration reducing cerebral perfusion, and osmotic shifts affecting brain cells.

It is crucial to understand that neurological symptoms indicate advanced DKA requiring immediate intervention. A patient who was communicating normally an hour ago may become unresponsive if treatment is delayed. Children are particularly vulnerable to cerebral edema (brain swelling) during DKA treatment, which is why pediatric DKA requires specialized management protocols.

DKA Can Mimic Stomach Flu

One of the most dangerous aspects of diabetic ketoacidosis is its ability to masquerade as common stomach illness. The combination of nausea, vomiting, and abdominal pain closely resembles viral gastroenteritis, food poisoning, or other gastrointestinal conditions. This similarity leads to delayed diagnosis in many cases, sometimes with tragic consequences.

People with type 1 diabetes should always check their blood glucose and ketone levels when experiencing gastrointestinal symptoms, even if they suspect a simple stomach bug. It is also important to note that actual stomach illness with vomiting and diarrhea can trigger DKA in people with diabetes by causing dehydration and making it difficult to eat normally. This creates a dangerous situation where the underlying infection provokes a metabolic crisis.

What Causes Diabetic Ketoacidosis?

Diabetic ketoacidosis is caused by severe insulin deficiency combined with elevated stress hormones. Common triggers include missed insulin doses, undiagnosed type 1 diabetes, infections, insulin pump failure, and severe illness. Without enough insulin, the body cannot use glucose and begins breaking down fat, producing toxic ketone acids.

The fundamental cause of diabetic ketoacidosis is inadequate insulin availability to meet the body's metabolic needs. This deficiency can be absolute, as occurs in type 1 diabetes or when insulin injections are missed, or relative, when insulin requirements surge during illness or stress beyond what is being provided. Understanding the specific triggers of DKA helps both patients and healthcare providers prevent episodes and recognize them early.

In people with established type 1 diabetes, the most common precipitant of DKA is omission or inadequate dosing of insulin. This may occur intentionally, often in adolescents struggling with the psychological burden of chronic disease management, or unintentionally due to forgetfulness, running out of supplies, or economic barriers to obtaining insulin. Studies consistently show that insulin non-adherence underlies 20-40% of DKA episodes.

Infections represent another major trigger, accounting for approximately 30-40% of DKA cases. When the body fights infection, it releases stress hormones that antagonize insulin action and stimulate glucose production by the liver. Common infections precipitating DKA include urinary tract infections, pneumonia, skin infections, and gastroenteritis. Patients often make the mistake of reducing or stopping insulin when they feel too sick to eat, not realizing that their insulin requirements are actually increased during illness.

Insulin Pump Problems

For patients using insulin pumps, equipment malfunctions represent a specific risk for DKA. Modern pump therapy delivers only rapid-acting insulin, with no long-acting background insulin as backup. If the pump catheter becomes kinked, dislodged, or blocked, insulin delivery stops completely. Without the reservoir of long-acting insulin that injection users have, pump users can develop DKA remarkably quickly – sometimes within 4-6 hours of pump failure.

Regular pump site inspection and rotation, along with protocols for checking ketones when unexpectedly high blood sugars occur, are essential safety measures for pump users. Many diabetes teams recommend that pump users keep backup long-acting insulin available for emergencies and know how to calculate doses if their pump fails.

Other Causes of DKA

Newly diagnosed diabetes frequently presents as DKA, particularly in children and young adults with type 1 diabetes. Before diagnosis, these individuals have progressive insulin deficiency without any treatment, leading inexorably toward ketoacidosis. Recognition of diabetes symptoms (thirst, urination, weight loss) before DKA develops can prevent this serious presentation, but public awareness remains inadequate in many communities.

Certain medications can increase DKA risk. SGLT2 inhibitors, a class of diabetes drugs that work by causing glucose excretion in urine, have been associated with atypical DKA presentations where blood glucose may be only mildly elevated despite significant ketoacidosis. Corticosteroids, commonly prescribed for various inflammatory conditions, dramatically increase insulin resistance and can precipitate DKA in susceptible individuals.

Severe physiological stressors including myocardial infarction (heart attack), stroke, pancreatitis, trauma, and major surgery can all trigger DKA by massively increasing counter-regulatory hormone release. These situations require careful glucose monitoring and often substantially higher insulin doses to prevent ketoacidosis.

When Should You Seek Emergency Care for DKA?

Seek emergency care immediately if you have diabetes and experience vomiting that prevents keeping fluids down, blood glucose above 300 mg/dL (17 mmol/L) that does not respond to insulin, moderate to large ketones, fruity breath odor, rapid deep breathing, confusion, or drowsiness. DKA can progress to coma within hours without treatment.

The decision to seek emergency care for suspected diabetic ketoacidosis should err on the side of caution, as delayed treatment significantly worsens outcomes. While mild hyperglycemia with low-level ketones may sometimes be managed with close home monitoring under healthcare provider guidance, any concerning symptoms warrant immediate evaluation. The consequences of delayed treatment are severe and potentially fatal.

Certain symptoms should trigger an immediate call to emergency services. Altered mental status – whether confusion, unusual drowsiness, difficulty arousing, or unresponsiveness – indicates severe DKA affecting brain function. Kussmaul breathing, the characteristic rapid and deep respiratory pattern, signals that the body is attempting to compensate for severe acidosis. The fruity acetone breath odor, while not always present, is highly specific for significant ketone accumulation.

Persistent vomiting creates a particularly dangerous situation because it prevents oral fluid intake needed to combat dehydration while also making it impossible to take oral diabetes medications. Additionally, the retching itself can worsen electrolyte imbalances. Any patient with diabetes who cannot keep liquids down for more than a few hours needs medical evaluation.

Blood glucose readings provide objective guidance for seeking care. Levels consistently above 300 mg/dL (17 mmol/L) despite appropriate insulin administration, especially with symptoms, require prompt evaluation. Some guidelines suggest emergency care when glucose exceeds 250 mg/dL (14 mmol/L) with moderate to large ketones and symptoms, as this indicates established ketoacidosis.

How Is Diabetic Ketoacidosis Diagnosed?

Diabetic ketoacidosis is diagnosed through blood tests showing high blood glucose (usually >250 mg/dL/14 mmol/L), elevated blood ketones (>3.0 mmol/L), and low blood pH (<7.3) or low bicarbonate (<18 mEq/L). Tests include blood glucose, blood or urine ketones, arterial blood gas, and comprehensive metabolic panel. Diagnosis can usually be confirmed within minutes in an emergency setting.

The diagnostic criteria for diabetic ketoacidosis have been established by major diabetes organizations and encompass three key biochemical abnormalities: hyperglycemia, ketonemia or ketonuria, and metabolic acidosis. While clinical suspicion based on symptoms is important, confirmation requires laboratory testing that can rapidly be performed in emergency departments and most urgent care settings.

Blood glucose measurement is typically the first test performed when DKA is suspected. Values usually exceed 250 mg/dL (14 mmol/L), though the previously mentioned euglycemic DKA associated with SGLT2 inhibitors may present with lower values. Point-of-care glucose meters provide results within seconds, allowing rapid assessment. However, these meters become less accurate at very high glucose levels, so laboratory confirmation is standard.

Ketone assessment can be performed using blood or urine testing. Blood ketone meters measuring beta-hydroxybutyrate have become the preferred method because they provide quantitative results and detect the most abundant ketone in DKA. Blood ketone levels above 3.0 mmol/L strongly suggest DKA. Urine ketone testing, while more readily available, detects acetoacetate rather than beta-hydroxybutyrate and can be falsely negative early in DKA or falsely positive during treatment when beta-hydroxybutyrate converts to acetoacetate.

Laboratory Tests for DKA

Arterial blood gas analysis provides critical information about the degree of acidosis. In DKA, the blood pH falls below 7.3 (normal is 7.35-7.45), with bicarbonate levels reduced below 18 mEq/L (normal is 22-28 mEq/L). The degree of acidosis correlates with DKA severity: mild DKA has pH 7.25-7.30, moderate DKA has pH 7.0-7.24, and severe DKA has pH below 7.0.

A comprehensive metabolic panel reveals the extent of electrolyte disturbances. Sodium levels may be low, normal, or high depending on the relative losses of water and sodium. Potassium levels require careful interpretation – while total body potassium is severely depleted in DKA, serum potassium may initially appear normal or even high due to acidosis shifting potassium out of cells. This can mask dangerous potassium deficiency that becomes apparent during treatment.

The anion gap, calculated from sodium, chloride, and bicarbonate values, is characteristically elevated in DKA due to ketone accumulation. Normal anion gap is 8-12 mEq/L, while DKA typically produces gaps exceeding 20 mEq/L. Following the anion gap during treatment helps assess response to therapy.

How Is Diabetic Ketoacidosis Treated?

DKA treatment requires hospitalization and involves three main components: intravenous fluids to correct dehydration, intravenous insulin to lower blood glucose and stop ketone production, and electrolyte replacement (especially potassium). Treatment is carefully monitored to prevent complications like cerebral edema and hypokalemia. Most patients improve within 12-24 hours with proper treatment.

Treatment of diabetic ketoacidosis is a medical emergency requiring close monitoring and typically intensive care unit admission for severe cases. The goals of treatment are to restore fluid volume, normalize blood glucose, clear ketones, correct electrolyte imbalances, and identify and treat any precipitating cause. Each component of therapy must be carefully orchestrated to avoid complications that can arise from too-rapid correction.

Fluid resuscitation is the first priority in DKA treatment. Patients are typically severely dehydrated, having lost an average of 6-9 liters of fluid through osmotic diuresis. Initial therapy involves rapid infusion of isotonic saline (0.9% sodium chloride) at rates of 1-1.5 liters per hour for the first 1-2 hours in adults, followed by slower rates guided by hydration status and urine output. Fluid replacement alone can substantially lower blood glucose by improving kidney filtration and diluting concentrated blood.

Insulin therapy is essential to halt ketone production and allow glucose to enter cells. Continuous intravenous insulin infusion is the standard approach in hospital settings, starting at approximately 0.1 units per kilogram per hour after adequate fluid resuscitation. The insulin infusion continues until ketoacidosis resolves (defined by closure of the anion gap and blood pH above 7.3), which typically takes 12-24 hours. Blood glucose should decrease by approximately 50-75 mg/dL (3-4 mmol/L) per hour.

Electrolyte Management

Potassium replacement is critically important and potentially life-saving. Despite often-normal initial serum potassium levels, total body potassium is severely depleted in DKA. As insulin therapy begins and acidosis corrects, potassium shifts back into cells, potentially causing dangerous hypokalemia with cardiac arrhythmia risk. Potassium replacement is initiated when serum potassium falls below 5.2 mEq/L, with the goal of maintaining levels between 4-5 mEq/L throughout treatment.

Bicarbonate administration remains controversial and is generally reserved for severe acidosis (pH below 6.9-7.0). While intuitively it might seem beneficial to directly treat acidosis with bicarbonate, studies have not shown improved outcomes, and risks include paradoxical worsening of intracellular acidosis, hypokalemia acceleration, and potential contribution to cerebral edema in children. Current guidelines recommend bicarbonate only in cases of life-threatening acidosis or severe hyperkalemia.

Monitoring During Treatment

Frequent laboratory monitoring is essential during DKA treatment. Blood glucose should be checked every 1-2 hours, with metabolic panel and blood gas assessment every 2-4 hours initially. When blood glucose reaches approximately 200 mg/dL (11 mmol/L), dextrose is added to intravenous fluids to prevent hypoglycemia while insulin is continued to fully resolve ketoacidosis. The transition back to subcutaneous insulin should overlap with the insulin infusion by several hours to prevent rebound hyperglycemia.

How Can You Prevent Diabetic Ketoacidosis?

Preventing DKA involves never skipping insulin doses, monitoring blood glucose regularly (especially when ill), checking ketones when blood sugar is high, following sick day guidelines, ensuring insulin pump function, and adjusting insulin doses appropriately during illness. Regular diabetes education and healthcare follow-up are essential prevention strategies.

Prevention of diabetic ketoacidosis is achievable in most cases through proper diabetes management, patient education, and adherence to established protocols during high-risk situations. Understanding that DKA develops when insulin delivery fails to meet metabolic demands allows patients and families to take proactive steps to maintain adequate insulin coverage.

The cornerstone of DKA prevention is never missing insulin doses. Even during illness when appetite is reduced or nausea prevents eating, insulin remains essential. In fact, insulin requirements typically increase during illness due to stress hormone release. Patients should work with their diabetes team to develop individualized sick day rules that specify insulin adjustment strategies for various scenarios.

Regular blood glucose monitoring provides early warning of developing problems. Current guidelines recommend checking blood glucose at least four times daily for most people with type 1 diabetes, with additional checks during illness or when symptoms suggest hyperglycemia. Morning glucose checks are particularly valuable, as DKA can develop overnight without the patient realizing symptoms until morning.

Sick Day Management

Sick day guidelines are protocols developed by diabetes teams to help patients safely manage diabetes during illness. Key principles include continuing insulin (never stopping it), checking blood glucose every 2-4 hours, testing ketones when glucose exceeds 250 mg/dL (14 mmol/L), maintaining hydration with sugar-free fluids, and knowing when to contact healthcare providers or seek emergency care.

For patients using insulin pumps, specific precautions help prevent pump-related DKA. These include checking the infusion site daily for signs of problems, changing the infusion set at recommended intervals, verifying pump function when unexpectedly high glucose occurs, and having backup supplies including long-acting insulin and syringes available. Many diabetes teams recommend checking blood glucose 2 hours after any infusion set change to ensure proper insulin delivery.

Ketone Monitoring

Home ketone monitoring provides crucial information during high-risk periods. Blood ketone meters are preferred over urine ketone strips for accuracy and speed. Testing should be performed when blood glucose exceeds 250 mg/dL (14 mmol/L), during illness, or when symptoms suggest DKA. Ketone levels guide action: low levels (<0.6 mmol/L) require continued monitoring, moderate levels (0.6-1.5 mmol/L) warrant increased insulin and fluids with close follow-up, and high levels (>1.5 mmol/L) require immediate medical consultation.

Special Considerations for Ketogenic Diets

Ketogenic or very low-carbohydrate diets (often called LCHF or keto diets) pose particular risks for people with type 1 diabetes. These diets intentionally induce nutritional ketosis through severe carbohydrate restriction, which can blur the line between normal dietary ketosis and developing ketoacidosis. The combination of deliberately elevated ketones and any insulin delivery problem can rapidly progress to dangerous DKA.

If considering a ketogenic diet with type 1 diabetes, close supervision by a diabetes specialist is essential. More frequent ketone monitoring, careful insulin adjustment, and clear parameters for seeking care should be established before starting such a diet. Many diabetes teams advise against ketogenic diets in type 1 diabetes due to increased DKA risk.

What Are the Complications of DKA?

DKA complications include cerebral edema (brain swelling, especially in children), hypokalemia (low potassium causing heart rhythm problems), hypoglycemia during treatment, acute kidney injury, and rarely death. Cerebral edema is the most serious complication in pediatric DKA, occurring in 0.5-1% of cases with high mortality. Proper treatment protocols minimize complication risk.

While modern treatment protocols have dramatically reduced mortality from diabetic ketoacidosis, the condition remains associated with significant complications that can occur both from the metabolic derangement itself and from therapy. Understanding these complications helps guide the careful, measured approach to DKA treatment that specialists employ.

Cerebral edema represents the most feared complication of DKA, particularly in children and adolescents. This brain swelling typically develops 4-12 hours after treatment initiation, when patients may otherwise appear to be improving. Warning signs include headache, altered consciousness, irritability, and neurological changes. The exact cause remains incompletely understood but may involve rapid fluid shifts during treatment. Cerebral edema occurs in 0.5-1% of pediatric DKA episodes and carries mortality rates of 20-25%.

Hypokalemia (low potassium) during treatment is common and potentially dangerous. As insulin drives potassium back into cells and acidosis corrects, serum potassium can drop precipitously. Severe hypokalemia causes muscle weakness, respiratory compromise, and life-threatening cardiac arrhythmias. Continuous cardiac monitoring and frequent potassium measurement during DKA treatment allow early intervention.

Hypoglycemia (low blood sugar) can occur during treatment if insulin continues without adequate glucose provision. As blood glucose normalizes, dextrose must be added to intravenous fluids while insulin continues to resolve ketoacidosis. Overly aggressive insulin dosing without glucose monitoring can result in dangerous hypoglycemia.

Acute kidney injury affects many patients with DKA due to severe dehydration reducing kidney blood flow. Most cases resolve with fluid resuscitation, but some patients require temporary dialysis. Pre-existing kidney disease increases this risk.