Recurrent DKA: Why Does Diabetic Ketoacidosis Come Back, and How Is It Prevented?

The second time is the one that stings. The first admission for diabetic ketoacidosis can be written off as bad luck, a stomach bug, a pump that failed overnight. But when the same fluorescent ward lights, the same drip stand and the same gently worried questions return a few months later, people start asking a harder question of themselves: why me, again?

That question deserves a better answer than a shrug. Recurrent DKA causes are rarely mysterious once someone takes the time to look. They tend to cluster into a short list of patterns, and most of those patterns can be interrupted. Some are mechanical, like a kinked cannula. Some are biological, like a chest infection. And some are deeply human, like running out of energy to manage an exhausting condition every single day.

This explainer walks through what the evidence says about why ketoacidosis repeats, who is most at risk, and the unglamorous habits that keep people out of hospital.

What is diabetic ketoacidosis, and what does recurrent actually mean?

Diabetic ketoacidosis, usually shortened to DKA, is a medical emergency in which the blood becomes acidic because the body is burning fat for fuel in the absence of enough insulin. Insulin is the hormone that lets glucose move from the bloodstream into cells. Without it, cells starve while glucose piles up outside them, and the liver responds by turning fat into acids called ketones.

Ketones in small amounts are harmless; many people make a few after an overnight fast. In DKA they accumulate faster than the body can clear them, tipping blood chemistry into acidosis, the clinical word for blood that has become too acidic to support normal organ function. Mayo Clinic notes that the condition can develop quickly, sometimes within 24 hours, which is why a mild upset in the morning can become a hospital admission by nightfall.

Recurrent simply means it has happened more than once. There is no single agreed cut-off in everyday clinical practice, but most diabetes teams start paying closer attention after a second episode within a year or two, because repetition usually points to a pattern rather than a one-off accident.

DKA is far more common in type 1 diabetes, where the pancreas makes little or no insulin. It can also occur in type 2 diabetes, especially during severe illness or with certain glucose-lowering medicines, and in forms of diabetes that are initially mislabelled. Each episode carries real risk: dehydration, dangerous shifts in potassium, swelling in the brain in rare cases, and a heavy toll on confidence. Understanding why it returns is the first step to making sure it does not.

How does DKA actually happen inside the body?

Picture insulin as the key that opens the door to every cell. When the key is missing, two things happen at once, and both make matters worse.

First, glucose cannot enter cells, so it stays in the blood. The kidneys try to flush the excess out, dragging water and salts with it. That is why early DKA feels like relentless thirst and frequent trips to the bathroom. Dehydration follows, and as fluid is lost, the blood becomes more concentrated and acids are cleared less efficiently.

Second, the body behaves as though it were starving, because from the cells’ point of view it is. The liver breaks down fat into ketones to provide an alternative fuel. Two of the main ketones, acetoacetate and beta-hydroxybutyrate, are acids. A third, acetone, is breathed out, which gives the breath a fruity or nail-polish smell that nurses learn to recognise from across a room.

Stress hormones pour fuel on the fire. Cortisol, adrenaline and glucagon are released during infection, injury, emotional stress or even dehydration itself, and all of them push the liver to release more glucose and make more ketones. This is why a person with diabetes can slide into DKA during a flu even if they take their usual insulin: the usual amount is no longer enough to match the surge in counter-regulatory hormones.

As acid builds up, breathing becomes deep and rapid in an effort to blow off carbon dioxide, nausea and vomiting set in, and the vomiting makes it even harder to drink fluids or keep medicines down. The loop closes on itself. Breaking it requires fluids and insulin given under close monitoring, which is why the MedlinePlus and NHS guidance treat DKA as a hospital condition, not a home one.

Recurrent DKA causes: why does diabetic ketoacidosis come back?

When diabetes teams review repeated admissions, the same handful of triggers appears again and again. Mayo Clinic lists missed insulin and illness or infection as the most common provocations for DKA, and the pattern holds for recurrence. The difference with repeat episodes is that the trigger often sits inside daily life rather than arriving from outside.

The table below summarises the main categories, how quickly each tends to act, and the practical counter-measure most guidance recommends.

Trigger category	Typical mechanism	Usual counter-measure
Missed or omitted insulin	No insulin means no brake on fat breakdown; basal insulin gaps are especially dangerous	Protect basal doses; identify why doses are skipped
Pump or delivery failure	Blocked, kinked or dislodged cannula stops rapid-acting insulin with no long-acting reserve	Check ketones early with unexplained highs; keep backup pens
Infection or illness	Stress hormones raise glucose and ketone production beyond usual insulin needs	Written sick-day plan; frequent ketone checks
Certain medicines	Steroids raise glucose; SGLT2 inhibitors can cause DKA with near-normal glucose	Review with prescriber; know the warning signs
Psychological and social factors	Burnout, eating distress, alcohol, access barriers lead to insulin omission	Screening and support alongside education

Notice that only one row is truly external. The rest involve insulin that was prescribed but did not reach the bloodstream, or needs that rose while the usual plan stayed still. That is good news in one sense: a trigger that lives in routine can be changed by changing routine. It also explains why the single most useful question after a repeat admission is not ‘what went wrong this time?’ but ‘what keeps going wrong?’

Why does DKA keep happening when insulin is missed?

Among recurrent DKA causes, missed insulin stands apart because it is both the most common and the least talked about. People often feel judged when it is raised, which makes honest conversation harder, which makes the next episode more likely.

The biology is unforgiving. In type 1 diabetes, the pancreas makes essentially no insulin, so there is no internal safety net. Long-acting, or basal, insulin provides a steady background level that keeps fat breakdown in check around the clock. Skip a mealtime dose and glucose rises uncomfortably; skip the basal dose and the brake on ketone production comes off entirely. The NHS describes DKA developing in people who have missed insulin doses, and basal gaps are the ones most clearly linked to ketoacidosis within a day.

Why do doses get missed? The reasons are rarely carelessness. Diabetes demands dozens of small decisions daily, and fatigue is real. Shift work scrambles routines. A supply runs out before a prescription is renewed. A teenager wants one evening of not being the person with diabetes. An adult who has had the condition for twenty years simply forgets, the same way anyone forgets a vitamin.

Some people deliberately omit insulin to lose weight, a pattern that clinicians recognise as a form of disordered eating specific to diabetes. It carries a high risk of repeated DKA and deserves compassionate, specialist support rather than a lecture.

The practical response is twofold. Teams try to make basal insulin as hard to miss as possible: alarms, pen caps that log timing, pairing doses with an anchored habit such as brushing teeth. And they ask, without blame, what gets in the way. Treating the obstacle, whether it is a prescription renewal system or burnout, tends to do more than repeating instructions that the person already knows by heart.

Can an insulin pump cause recurrent DKA?

Insulin pumps deliver small, continuous amounts of rapid-acting insulin through a thin cannula under the skin, replacing the need for long-acting injections. That design is their strength and their vulnerability. Because the pump supplies only rapid-acting insulin, there is no long-acting reserve in the body. If delivery stops, insulin levels fall within hours and ketones begin to climb.

Delivery can fail silently. A cannula kinks under the skin. A set pulls partly out during sleep. An air bubble occupies the tubing. Insulin left in a hot car loses potency. The pump screen may show a dose delivered while nothing actually reaches tissue. Mayo Clinic lists problems with insulin pump therapy among recognised DKA triggers, and the pattern in recurrent cases is often a user who trusts the device slightly more than the device deserves.

The warning sign is a glucose reading that stays high despite correction doses from the pump. Pump education programmes typically teach a simple rule: an unexplained high that does not respond to one correction should prompt a ketone check and, if ketones are present, an injection with a pen or syringe and a full set change. Waiting to see whether the next correction works is where the hours slip away.

Closed-loop or automated systems that adjust delivery using a continuous glucose monitor reduce some risk by alarming on persistent highs, but they cannot push insulin through a blocked cannula. The backup pen in the drawer remains essential equipment.

People with repeated pump-related DKA are usually asked to review their site-change routine, cannula type and troubleshooting steps with the pump team. In some cases the team may suggest a period back on injections while the pattern is understood. That is not a punishment; it is a way to remove one variable so the others can be seen clearly.

Infections, illness and stress hormones: the classic triggers

A urinary tract infection. A chest infection. Gastroenteritis that empties the stomach and the will to live for 48 hours. These are the oldest known DKA triggers, and they explain a large share of first episodes as well as repeats.

During infection the body releases cortisol, adrenaline and glucagon. Each tells the liver to release stored glucose and to make new glucose, preparing the body to fight. In someone without diabetes the pancreas simply produces more insulin to match. In someone with type 1 diabetes, the usual injected amount suddenly covers far less than it did yesterday. Glucose rises, ketones follow, and the person, feeling awful, may eat little and conclude that less insulin is needed. The opposite is usually true.

Vomiting adds a trap of its own. Someone who cannot keep food down may reason that insulin without food will cause a dangerous low. Sick-day guidance from the NHS and from diabetes educators is consistent on this point: insulin should never be stopped during illness, even when eating is impossible, because the body still needs it to control ketones. How much to take, and when to adjust, is a decision for the care team’s written plan and for a phone call if the plan is unclear.

Stress hormones rise with more than infection. Surgery, injury, a heart attack, severe emotional shock and pregnancy all raise insulin requirements. Steroid medicines, such as those prescribed for asthma flares or inflammatory conditions, mimic cortisol and can raise glucose markedly within a day of starting.

The pattern in recurrent DKA is often a person whose illnesses are not unusually frequent but whose response to the first signs of illness is slow. Earlier ketone testing and earlier contact with the team, rather than fewer infections, is the realistic lever to pull.

Euglycemic DKA and SGLT2 inhibitors: ketoacidosis with near-normal glucose

One of the more surprising recurrent DKA causes involves a class of glucose-lowering tablets. SGLT2 inhibitors work by making the kidneys excrete more glucose in the urine. They are widely prescribed in type 2 diabetes and, for their heart and kidney benefits, in some people without diabetes at all.

Because glucose leaves through the kidneys, blood glucose can look reassuringly normal even when the body is short of insulin and producing ketones. This is called euglycemic DKA: ketoacidosis with a blood glucose that is only mildly raised or close to the usual range. The usual mental alarm, a very high glucose reading, never sounds. People and sometimes clinicians are lulled into thinking nothing serious is happening while nausea, abdominal pain and rapid breathing creep in.

Regulatory agencies and clinical guidance recognise this risk, and several situations raise it further: reduced food intake, very low-carbohydrate diets, prolonged fasting, dehydration, surgery, heavy alcohol use and acute illness. People with type 1 diabetes taking an SGLT2 inhibitor off-label face a higher risk, which is why most guidance is cautious about that use.

The protective habit is to test ketones whenever feeling unwell, regardless of the glucose number, and to treat ketones in the blood as the signal that matters. Most teams also advise pausing these tablets around planned surgery, during acute illness or when unable to eat, but that instruction has to come from the prescribing clinician who knows the person’s full picture. Nobody should stop or restart a prescribed medicine based on an article.

For someone with repeat DKA who takes an SGLT2 inhibitor, a frank review with the prescriber about whether the benefits still outweigh the risks is a reasonable and routine conversation to request.

The hidden drivers: mental health, eating distress, alcohol and access

Diabetes teams who study repeat admissions learn quickly that the chemistry is the easy part. The harder part is the life around it.

Diabetes distress, the exhausted, resentful feeling that comes from managing a condition that never takes a day off, is common and under-recognised. It is not the same as depression, though the two overlap, and it strongly predicts missed doses. Depression itself reduces the energy to inject, test and plan. Anxiety about hypoglycaemia leads some people to run their glucose deliberately high, shaving insulin until they sit permanently closer to ketosis.

Disordered eating in diabetes, including deliberate insulin restriction to lose weight, carries one of the highest risks of recurrent DKA. It thrives on secrecy and shame, which means a team that asks gently and without judgement is more likely to hear the truth than one that simply reviews the glucose log.

Alcohol is a double hazard. Heavy drinking suppresses the liver’s glucose release, can trigger a separate alcoholic ketoacidosis, and reliably disrupts the routine of injecting and eating. Recreational stimulants raise stress hormones and suppress appetite in ways that mimic illness.

Then there are the practical barriers that have nothing to do with willpower: insulin that cannot be collected because of work hours, a pharmacy that runs out, housing instability that makes refrigeration impossible, a language barrier at every appointment. Where these drive insulin gaps, the clinical fix is social, not pharmacological, and the care team can often connect people with the right support once the problem is named.

The point is not that recurrent DKA is a psychological condition. It is that insulin only works if it enters the body, and the reasons it fails to do so are usually human rather than biochemical.

Who is most at risk of recurrent DKA, and who is usually offered extra support?

Some people are more likely than others to see ketoacidosis return, and knowing the risk groups helps teams target help before the next admission rather than after.

Adolescents and young adults with type 1 diabetes carry a well-recognised higher risk. The transition from paediatric to adult care, moves away from home, irregular sleep and the ordinary turbulence of growing up all make routine harder to hold. People whose first DKA episode was their diagnosis and who are still learning the condition are also vulnerable in the early months.

Anyone using an insulin pump has a structural risk because of the absence of long-acting insulin, regardless of how experienced they are. People taking SGLT2 inhibitors, those on long-term or repeated steroid courses, and people with recurrent infections, such as frequent urinary infections, sit on the list as well. So do people with coexisting mental health conditions, eating disorders or substance use, and people facing barriers to collecting or affording supplies.

Who is usually asked to wait, or offered a different pathway? Teams tend to hold back on starting pump therapy, or pause it, in someone with very recent repeated DKA until the underlying pattern is understood, because adding a device with no insulin reserve to an unstable situation can raise risk rather than lower it. Similarly, SGLT2 inhibitors are often avoided or stopped in people with type 1 diabetes or a history of ketoacidosis. Intensive technology is generally paired with intensive education rather than offered on its own.

After a second episode, most services offer a structured review: a look at insulin storage and supply, a pump check if relevant, screening questions about mood and eating, and a refreshed sick-day plan. Being placed in a higher-risk group is not a label of failure. It is the system flagging that this person deserves more than a standard follow-up letter.

How to prevent DKA: the sick-day rules that actually work

Prevention of recurrent DKA is not glamorous. It is a short list of habits, practised until they feel automatic, plus a written plan for the days when thinking clearly is hardest.

The first rule is the one every diabetes educator repeats: never stop insulin. Illness, vomiting, loss of appetite and fasting all raise the need for insulin rather than lowering it. Basal insulin, in particular, should continue even when nothing is eaten. Adjustments to amounts belong to the care team’s plan.

The second is to test ketones early and often when unwell or when glucose is unexpectedly high. Blood ketone meters give a direct reading; urine strips lag behind by a few hours but are better than nothing. The NHS and Cleveland Clinic both advise checking ketones during illness and whenever glucose is high, with the specific thresholds set by the individual’s team. A single reading is less useful than a trend, so repeating the test every few hours during illness, as the sick-day plan specifies, is the habit that catches problems while they are still manageable at home.

The third is fluids. Dehydration concentrates acids and worsens the kidneys’ ability to clear ketones. Sugar-free fluids when glucose is high, and small amounts of carbohydrate-containing fluids when unable to eat, keep both hydration and energy intake going.

Fourth, keep a backup. Pump users need in-date pens and needles. Everyone needs spare insulin stored correctly, a working ketone meter with in-date strips, and the clinic’s out-of-hours number saved somewhere obvious.

Finally, treat the sick-day plan as a document to review annually and after every admission. People change, regimens change, and a plan written at diagnosis may no longer match the insulin in the fridge. A ten-minute review with the team costs little and removes a surprising number of gaps.

What do the days and weeks after a DKA admission usually look like?

Hospital treatment for DKA follows a well-rehearsed sequence: intravenous fluids to restore volume, insulin given by infusion to switch off ketone production, and careful replacement of potassium and other salts that shift as the acidosis corrects. Blood is checked frequently. The acute phase usually resolves within a day or so once treatment begins, though MedlinePlus notes that the time to recovery depends on how severe the episode was and what triggered it.

The transition back to usual injections or pump therapy happens before discharge. This handover, when the infusion stops and the long-acting insulin takes over, is a known moment of vulnerability; teams overlap the two deliberately so that no gap in insulin occurs.

The first week at home often feels flat. Tiredness lingers, appetite is unpredictable, and glucose can swing while the body recovers from illness and stress hormones settle. Many people describe a wariness around food and insulin, testing more than usual, afraid of a repeat. That vigilance is understandable and tends to ease.

Most services arrange a follow-up contact within a few weeks. This is the appointment where the real work on recurrence happens: reviewing what triggered the episode, checking pump sites or injection technique, refreshing the sick-day plan, and asking about mood, eating and supply. If a medicine such as an SGLT2 inhibitor or a steroid contributed, the prescriber reviews it then.

Over the following months, the aim is to rebuild confidence rather than fear. People who have had two or more episodes may be offered a structured education course, closer contact with a diabetes specialist nurse, or psychological support. None of this is a verdict on how well someone has coped. It reflects the evidence that recurrence is best prevented by addressing the pattern, and patterns take more than one conversation to change.

What people often get wrong about recurrent DKA causes

Myths around ketoacidosis are stubborn, and several of them actively contribute to repeat episodes. Clearing them up is part of prevention.

If I am not eating, I do not need insulin. This is the most dangerous misunderstanding. The body produces glucose and ketones whether or not food arrives, and during illness it produces more. Insulin is needed to control that process. Stopping it when unwell is a direct route to DKA.

My glucose is normal, so I cannot have ketoacidosis. With SGLT2 inhibitors, during pregnancy, after alcohol or after prolonged fasting, DKA can occur with glucose near the usual range. Ketones, not glucose, are the test that rules it in or out.

My pump said it delivered the dose, so the insulin is in. A pump records what it attempted, not what reached tissue. A blocked or dislodged cannula produces a perfectly normal delivery log and a steadily rising glucose.

DKA only happens to people who are careless. Infections, steroid courses, pump failures and surgery provoke DKA in meticulous people. Where insulin is omitted, the reasons are usually exhaustion, distress or access, not indifference.

Type 2 diabetes does not get DKA. It is less common but well documented, particularly during severe illness, with certain medicines, and in forms of diabetes that are later reclassified as type 1.

Urine ketone strips are as good as blood testing. Urine reflects ketone levels from several hours earlier. Blood ketone meters show the present, which matters when the situation can change within a day.

One episode means the next is inevitable. Recurrence follows patterns, and patterns can be changed. Most repeat admissions trace to a handful of modifiable triggers, which is exactly why the post-admission review matters so much.

Questions to ask your care team after a repeat episode

A follow-up appointment after DKA can feel like a debrief after an exam nobody wanted to sit. Arriving with questions turns it into something more useful. These are the ones diabetes educators most often wish people would ask.

• Looking at this episode and the previous one, what do you think the common thread was?
• Is my current insulin regimen still the right fit for how my days actually run, including shift patterns, sleep and meals?
• What exact ketone level should prompt me to call, and what level means I should go to the emergency department without waiting?
• Can we rewrite my sick-day plan together now, so it reflects the insulin I am using today?
• If I use a pump, what is the step-by-step routine when a glucose reading will not come down, and do I have everything I need for an injection backup?
• Are any of my medicines, including tablets for other conditions, raising my DKA risk, and is that something the prescriber should review?
• How should I handle insulin on days when I cannot eat or keep fluids down?
• Is there a way to make my basal insulin harder to miss, such as reminders, a connected pen or a change in timing?
• Can we talk about how I have been feeling about diabetes lately, and is there support available if it has been heavy?
• If supply or collecting prescriptions is part of the problem, who can help me sort that out?
• Would a continuous glucose monitor or a structured education course make sense for me, and what would the pathway be?
• Who do I contact out of hours, and what information will they want from me when I call?

Write down the answers. A sick-day plan that lives only in memory is the first thing to vanish when a fever hits. The decisions about insulin, devices and medicines belong with the team; the questions are how you shape them.

When to call your doctor: red-flag signs of developing ketoacidosis

Ketoacidosis rewards early action. The difference between a phone call and an intensive care admission is often a matter of hours, and the signs are recognisable once known. This is not a self-diagnosis checklist; it is a guide to when to stop watching and start calling.

Call your diabetes team or out-of-hours service the same day if:

• Your blood glucose stays high despite correction and you have ketones in blood or urine at the level your plan flags as concerning.
• You are unwell with an infection, fever or vomiting and are unsure how to adjust insulin or cannot keep fluids down.
• Your pump has failed or you suspect a delivery problem and ketones are present.
• You take an SGLT2 inhibitor and feel unwell with nausea or abdominal pain, even if glucose looks normal.

Go to the emergency department or call emergency services without delay if:

• Vomiting is repeated and you cannot keep fluids down for more than a few hours.
• Breathing becomes deep, rapid or laboured, or your breath smells fruity.
• You have severe abdominal pain, confusion, unusual drowsiness or difficulty staying awake.
• Ketones are high and rising despite following your sick-day plan.
• A child or young person with diabetes is vomiting, unusually sleepy or breathing fast.

The NHS, Mayo Clinic and MedlinePlus all describe DKA as a condition that needs hospital treatment, and none advise managing moderate or high ketones alone at home. If in doubt, make the call. Diabetes teams would far rather hear from someone three times who turns out to be fine than once from someone who waited.

Every decision about insulin, devices and medicines rests with the people who treat you. What this article can do is make sure the conversation starts earlier, with better questions, and before the ward lights come back on.

Frequently asked questions

Why does DKA keep happening to me even though I take insulin?

Usually because the insulin taken no longer matches what the body needs at that moment. Infection, steroids, dehydration and stress all raise insulin requirements, so the usual amount falls short. Pump delivery can fail silently, and basal doses can be missed without anyone noticing. A structured review with your diabetes team after each episode is the most reliable way to find the specific pattern behind your recurrences.

What are the most common DKA causes in type 1 diabetes?

Missed or omitted insulin and infection or illness are the two most common causes identified in clinical guidance. Others include insulin pump failure, steroid medicines, surgery, pregnancy, heavy alcohol use and newly diagnosed diabetes that has not yet been treated. In recurrent cases, gaps in basal insulin and psychological or practical barriers to taking it are found more often than unusual infections.

How to prevent DKA when I have a stomach bug and cannot eat?

Continue insulin, especially basal insulin, test ketones every few hours as your sick-day plan directs, and keep sipping fluids. Illness raises insulin needs even when no food goes in. If vomiting prevents fluids for more than a few hours, or ketones rise despite following the plan, contact your team or seek emergency care. Specific insulin adjustments come from your prescriber’s written plan, not from general advice.

Can SGLT2 inhibitors cause euglycemic DKA, and how would I know?

Yes. SGLT2 inhibitors make the kidneys excrete glucose, so blood glucose can look near-normal while ketones build up. Warning signs are nausea, vomiting, abdominal pain, unusual tiredness and rapid breathing without the very high glucose people expect. If you take one of these tablets and feel unwell, test ketones and contact your care team. Decisions about pausing or stopping the medicine belong with your prescriber.

Can you get DKA with normal blood sugar?

You can. This is called euglycemic DKA and occurs most often with SGLT2 inhibitor tablets, during pregnancy, after heavy alcohol use, or after prolonged fasting or very low-carbohydrate eating. The acidosis and ketone build-up are the same as in classic DKA; only the glucose reading is misleading. This is why testing ketones whenever you feel unwell, regardless of glucose, is a core prevention habit.

How quickly does DKA develop?

Mayo Clinic notes that DKA can develop quickly, sometimes within 24 hours, and in pump users who lose insulin delivery the process can begin within hours. Early signs are thirst, frequent urination and tiredness, followed by nausea, abdominal pain and rapid breathing. Catching the trend early with ketone testing is what turns a potential admission into a phone call and a plan.

Does an insulin pump increase the risk of recurrent DKA?

Pumps carry a specific structural risk because they deliver only rapid-acting insulin, leaving no long-acting reserve if the cannula blocks or dislodges. The risk is manageable with prompt ketone testing when glucose will not come down, immediate backup injections when ketones appear, and a full set change. Whether a pump is the right tool after repeated DKA is a judgement your diabetes team will make with you.

Why do teenagers and young adults get recurrent DKA more often?

Adolescence and early adulthood bring disrupted routines, moves away from home, irregular sleep and the transition from paediatric to adult services, all of which make consistent insulin harder. Diabetes distress and body-image pressures also peak in these years. Clinical guidance recognises this group as higher risk and most services offer closer follow-up and tailored support rather than standard appointments.

Is recurrent DKA a sign that my diabetes is getting worse?

Not necessarily. Recurrent DKA usually reflects a repeating trigger, such as missed basal insulin, pump problems, a medicine or an unaddressed source of distress, rather than a change in the underlying disease. It does signal that the current plan is not holding, which is why teams treat a second episode as a prompt for a full review rather than a judgement about how well someone is coping.

What should be in a sick-day plan to prevent DKA coming back?

A good plan states that insulin is never stopped, how often to test glucose and ketones when unwell, which ketone readings should prompt a call and which mean emergency care, what fluids to drink, how to handle days when eating is impossible, and the exact numbers to phone day and night. It should be written down, reviewed annually and updated after any admission or change of insulin.

References

• MedlinePlus: Diabetic ketoacidosis
• NHS: Diabetic ketoacidosis
• Cleveland Clinic: Diabetic ketoacidosis (DKA)
• CDC: About diabetic ketoacidosis

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.