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Diabetic Ketoacidosis: myths, tips, and lesser known facts

About one in four newly diagnosed persons with type 1 diabetes (and some type 2’s) will present in diabetic ketoacidosis (DKA) to a doctor’s office, urgent care facility, or emergency department. If not diagnosed and proper treatment started, DKA can be deadly. DKA is often misunderstood by persons with diabetes. Diabetic ketoacidosis is complex and easy to misunderstand by lay and professionals alike. The following is a practical explanation of what DKA is, and what it is not. I also dispel some common myths and provide practical tips to prevent or minimize DKA recurrence. It's not intended to be comprehensive, but rather to point out some important (at least to me) facts and perspectives about this potentially preventable condition. I hope you find it informative.

This IS a lengthy post. Feel free to bookmark it and read over time as needed. It’s intended to be a reference for you.

As we start, consider the following:

Which of the following statements are true and which are myths about DKA:

1. Overeating (carbs or anything else) causes DKA.

2. Nausea and vomiting must be present.

3. Persons with diabetes who are sick or stressed typically require less,

not more insulin.

4. All ketones are bad.

5. DKA only happens when I frequently omit scheduled insulin, use

damaged insulin, or have an insulin pump malfunction.

6. Insulin alone treats severe cases of DKA.

The answers are found at the end of this post, PLUS some bonus DKA prevention tips.


Type 1 diabetes results from a loss of ability to produce enough of the hormone called insulin. In most cases the immune system attacks the insulin making cells, called beta cells. There is considerable research about what triggers this destruction to happen. Some researchers believe the immune system mistakenly believes the beta cells to be foreign and begins a highly targeted attack to eradicate them. We know this can take weeks (probably months) to years to result in diabetes. Some adults may take years to decades to lose enough beta cells to cause the diabetic state to occur. Another theory gaining in acceptance is that the beta cells somehow begin to produce a defective protein which attracts an immune system attack. There are probably many causes that trigger this process of destruction. It would be unwise to believe only one reason exists for triggering type 1 diabetes. It is a fact that half of persons with type 1 diabetes are diagnosed after 30 years of age.

These insulin-making beta cells are in the core of a ball or cluster of hormone producing cells known as the islets of Langerhans. Approximately 1 million islets are embedded throughout the human pancreas. They are unevenly distributed throughout the organ. For reference the pancreas is located behind the stomach. The job of the pancreas is to assist the process of human digestion and proper conversion of food into cellular energy for growth or powering organs and tissues. In addition to insulin, the pancreas makes dozens of other hormones and chemical messengers. One of these other hormones is called glucagon. It is made and released by cells located next to beta cells, called alpha cells. More about glucagon and its role in DKA later.

With a dwindling insulin ability due to an ongoing autoimmune attack, the body is less capable of managing the products of digestion or balancing the internal chemical environment of the body. Before any symptoms occur, the blood sugar level of a person destined to develop type 1 diabetes may spike upwards with meals, but slowly return to normal afterwards. This is what is defined as ‘impaired glucose tolerance’. Frank diabetes occurs gradually in most persons. Beta cell damage and destruction is painless. The usual patient only ‘feels’ the final stages of this loss of insulin producing ability. Increased peeing and drinking are the earliest signs. With time, weight loss happens despite a good appetite. By the time the first signs or symptoms of diabetes are apparent, most of the ability to make insulin has been lost (80-90%).

When insulin levels are low, glucose (sugar) is less able to enter certain insulin responsive tissues. This results in a blood sugar traffic jam in the bloodstream. Sugar concentrations will rise within the blood to higher than normal levels. Early on, this may cause few to no symptoms. As more insulin ability is lost, the sugar levels rise to ranges which may start to create signs which might get noticed by the person or an astute observer (parent or spouse). As sugar gets backed up in the bloodstream, it also changes the concentration of water in the blood (thickens it). This measure is known as osmolality. The body prefers a balanced level of osmolality in the blood and will take steps to maintain it through a complex biological control system. One method is to increase the sense of thirst to get more water into the blood by drinking liquids more often. As water enters the bloodstream it acts to dilute the sugar levels. A more normal level of osmolality is achieved. Sugar levels fall since there is now more water (a larger total amount of blood volume) for the sugar to distribute itself within.


Two of the many jobs of our kidneys are to rid our bodies of the ‘biological exhaust’ of our metabolism and maintain a proper pH (acid-base) level in the bloodstream. The lungs play a role in this pH balancing act as well. In diabetes as sugar levels rise, the kidneys can eliminate some excess sugar by adding it to the urine. This fact formed one the first at home methods to monitor diabetes control: the urine glucose test. It was my first diabetes self-monitoring tool. Blood sugar monitoring, the A1C and now CGM has largely moved urine sugar testing to the history books. In general, the kidneys will “spill” sugar in some amount once the blood sugars exceed a value between 180-200 mg/dL (10-11 mmol/L). In persons with known diabetes, that level is at the upper limit since diabetic kidneys become more efficient at holding on to the sugar. When blood sugar levels exceed the ability of the kidneys to reclaim it, sugar (glucose) enters the urine. In this situation, each sugar molecule (glucose) must be escorted in the urine with a molecule of water. Therefore, as sugar levels rise, and the kidneys pass sugar out into urine. The cost is an ongoing loss of water. The amount of urine (it’s volume) increases. We notice this as someone “peeing a lot”.

Meanwhile in the body’s metabolic control center, the brain, the rising osmolality caused by dropping water levels triggers the sense of thirst. The mechanics of this are complex and involve more hormones and chemical messengers plus properly formed brain centers Thirst is a powerful defense against dehydration. Assuming the person has easy access to water or other fluids, the ongoing water being lost through the kidneys is replaced, at least for a while, by more frequent drinking. When you think back to the time before your diagnosis, there was a lot of drinking and peeing going on. You can see where persons who can’t easily get water on their own (infants, toddlers, the elderly) would quickly run into trouble.

Increased thirst and peeing represents the body’s attempt to fix and abnormal situation (high blood sugar). As the ability to produce insulin continues to dwindle, the absence of the growth promoting effects of insulin become increasingly noticeable. Insulin is a body building hormone. Muscle, fat and the liver are all insulin responsive tissues or organs. Without insulin to promote energy (sugar) entering insulin sensitive tissues, the process of growth stalls. Chemical reactions involved with cell growth slow down. The most obvious sign is losing weight. This comes from loss of body fat and muscle. Weight loss prior to diagnosis of diabetes is a common sign.

Without enough insulin, tiny organelles within cells called mitochondria begin to digest fat stores located within each cell. Fat represented a form of stored energy. The energy contained within a molecule of fat is denser and more powerful than a molecule of sugar. Fat can be likened to an energy savings account whereas glucose is like the dollars in your wallet. The cells don’t see sugar energy coming in due to the lack of insulin to promote the process of cellular sugar entry. Converting fat to energy does not require as much insulin. It’s a metabolic “plan B” to keep our body’s running when food energy is scarce.

With insulin lacking, the cell’s answer to this blockade is to take matters in their own hands and tap into internal energy stores. The mitochondria inside cells begin to chip away at long fat molecules, clipping them apart into smaller segments known as free fatty acids, or FFA’s. These fat fragments are used to generate an alternate source of usable energy since sugar is unavailable. FFA’s increase in the bloodstream. The liver removes FFA’s and chemically alters them into substances known as ketones. Therefore, ketones are a group of chemicals derived from fat breakdown. Acetone, acetoacetic acid and beta-hydroxybutyrate are the main ketone metabolites, but there are others minor ones.

Persons who practice low carb high fat eating seek to create a ketone positive environment by lowering insulin levels by carefully reducing carbohydrate eating and encourage ketone production from the FFA’s generated by digestion of dietary fat. Insulin acts to promote fat creation as well as sugar entry into cells. Low levels of insulin, or insulin rendered less effective by the presence of anti-insulin substances, flips a metabolic switch which causes fat to get broken down by mitochondria (see above) in addition to slowing down sugar entry into cells.

Ketones don’t require insulin to get inside cells and power cellular functions. It makes them an ideal sugar replacement when sugar is not available or can’t enter cells normally like what happens in diabetes. Ketones are not as “highly energetic” as glucose (sugar) but are still very helpful to meet basic energy needs when sugar (glucose) is unable to properly enter cells.

All this background is important to understand DKA. When insulin ability falls to very low levels, the resulting higher blood sugars trigger an ongoing loss of body water as sugar levels literally draw water out of cells themselves. This water enters the bloodstream. Unfortunately, this new water will also get swept out of the body through the urine as described above. Fortunately, as the newly emerging person with diabetes retains the capacity to find and drink fluids (usually water), then a new balance will be created. But that delicate balance will only last if access to fluids (water) is maintained and acid build up in the body is not too great.


The stage is now set for DKA. Unless someone notices the unusual pattern of thirst, frequent urination and weight loss (from water and losing real body tissue) all that is now needed is a trigger. The final ‘spark’ that starts a cascade of events resulting in DKA could be any of several things.

Besides a lack of insulin, there are many other hormones which typically increase. These hormones act to open the door for DKA to develop. Two of those anti-insulin hormones are glucagon and epinephrine. Years ago, it was shown that lack of insulin alone is insufficient to rapidly trigger DKA. A rise in glucagon and epinephrine typically create the DKA ‘spark or accelerant’ when insulin levels are low or insufficient enough. If these hormones are artificially blocked when insulin levels are low, DKA does not quickly happen, or at least happens very slowly. It reminds us that low insulin levels alone don’t pitch us into DKA. Other conditions must be met.


A low insulin level needs an accomplice to start the DKA wildfire. With this awareness, you might wonder what situations might create a conducive environment for DKA to explode?

Dehydration is a powerful inducer of DKA when insulin levels are insufficient. All stress hormones are present in higher amounts when someone is dehydrated (including glucagon and epinephrine, plus many others). If someone with diabetes comes down with any kind of viral or bacterial infection which interferes with their ability to maintain good water intake, or independently raises stress hormones, DKA could happen if insulin action is not sufficient enough to counteract the effect. Most stress hormones are anti-insulin in their actions. The person with diabetes must know how to counteract them by increasing insulin dosing based on a good knowledge of so-called ‘sick day’ self-management methods. Another defense is to have good communication with a diabetes team who can walk you through the next steps at the earliest stages, before the situation gets out of control.

Some medications can also contribute to stress hormone environment and usher in DKA. Oral or injected glucocorticoid medications (steroids) are often used to treat inflammatory conditions like asthma and arthritis. They block the effect of insulin and can result in a significantly higher daily insulin need. Often insulin needs can increase over 100% of normal. Each steroid’s effect varies with the amount of steroid, its potency and how it’s administered. Topical and inhaled steroids are usually less impactful on blood sugar levels.


DKA is a special form of dehydration. In persons without diabetes, depleted water in the body may result from vomiting, diarrhea, huge urinary losses, lack of access to water, increased water loss (excessive sweating, hot weather), or blood loss (blood is largely water) with inadequate replacement. In these cases, the water lost from the non-diabetic body comes largely from the blood (intravascular water) and the water stored between the cells (called the interstitial water). In DKA, water is also lost from inside the cells themselves. Very few types of dehydration can make that same claim (read below).

Why does this happen? Sugar trapped in the bloodstream (since insulin is lacking) pulls water out of cells, like a sponge. This water expands the volume of the blood (a ‘good’ thing). But this water is then promptly whisked away out of the blood and into the urine. Remember, the kidneys are trying to lower blood sugar levels by flushing excess sugar into the urine when the blood sugar level is at least over 180 mg/dL (10 mmol/L).

Extremely high blood sugars are sometimes measured during a case of DKA. Blood sugars over 2,000 mg/dL (111 mmol/L) have been reported. As mentioned earlier, the kidneys do their best to rid the body of some excess sugar which accumulates in the bloodstream due to the lack of insulin. For the kidneys to operate as ‘sugar pumps’, they must be supplied by enough blood flow to create effective urine. In states of dehydration, the body tries to protect what water it still has by temporarily directing blood away from the kidneys and towards more ‘important’ organs like the heart and brain. In doing this, blood sugar accumulates to very high levels since sugar simply keeps building up in a dwindling pool of water (the shrinking bloodstream). Blood sugar is expressed as an amount of sugar in milligrams (mg) dissolved in a certain amount of fluid mainly water) expressed as deciliters (dL). As the amount of sugar (in milligrams) increases due to an ongoing lack of insulin, levels rise even higher since the kidneys can’t generate enough urine to export extra sugar.

In general, two healthy human kidneys can maintain a blood sugar level of around 300 mg/dL (16.7 mmol/L) in the complete absence of insulin action. To do this there must be adequate water in the blood. This fact is useful to know when blood sugar levels are above this range. Many astute persons with diabetes know that staying well hydrated can act to lower sugar levels even when insulin levels are low or ineffective.


In usual cases of human dehydration, the amount of water in the blood is depleted and water in cells is preserved. Dehydration is still present within the body, but it’s where the water is being removed from that makes DKA such a fascinating condition to prevent and manage. DKA is what is called an intracellular dehydration as opposed to many other forms of body water loss known as extracellular dehydration. This is vital to understand when doctors manage DKA. Intracellular dehydration is the root cause of one of the deadliest complications of DKA: brain swelling, also known as cerebral edema.

If the body adjusts to having high sugars for a prolonged period, the brain prevents shrinkage by generating special particles inside brain cells to offset the water pulling forces created by the high sugars in the bloodstream. When DKA occurs and treatment starts, this involves replacing water and insulin through an IV (in hospital) or orally (liquids) and with injected rapid-acting insulin. But if the blood sugar is lowered too quickly (orally or with IV fluids), it upsets a delicate balance. The brain cells will be prone to absorb water from the blood and not the other way around. Overly aggressive insulin therapy can also lower sugar levels too quickly and further add to the osmotic imbalance between the blood and the brain. As the brain swells during treatment, it often does so after therapy has been started for several hours or longer. Research has shown that there is some mild brain swelling in 95% of all DKA cases even when treated properly. But for uncertain reasons, some persons are at higher risk for a deadlier severe complication known as severe cerebral edema. In part cerebral edema can be a result of overly aggressive medical management of DKA. But, cases of deadly cerebral edema have been known to happen even when medical treatment has been carefully administered and meticulous. Therefore…the best treatment for DKA is and always will be PREVENTION. The diabetes sick day rules are the best start.

Another complication of DKA are changes in the acid-base levels in blood. Normally our blood has a neutral pH, about 7.4. The ketones overproduced in DKA are known weak metabolic acids. We always have some ketones in our bloodstream at any point in time. It’s just a matter of how much. In DKA, the rapid breakdown of body fat into free fatty acids rushing into the bloodstream results in a tidal wave of ketones produced by the liver. These ketones may be called “weak” acids, but in large quantities ‘weak’ acts like ‘strong’ by their sheer numbers. A resulting acid imbalance occurs in the blood. As acid levels increase, their impact on the blood pH is offset by special anti-acid buffering systems in the blood. One of these substances is called bicarbonate. There are other buffer systems as well. In DKA, ketones are produced in such large amounts that they overwhelm the body’s normal buffering system. This results in a dropping of the blood pH to acidic levels (usually below 7.3).

Another byproduct of massive ketone production are substances called prostaglandins. One of these is notorious for causing nausea and vomiting by how it impacts the intestines and the process of human peristalsis. Glucagon is also present in large amounts during DKA. It can induce nausea and vomiting.

Part of the agreed upon medical definition of DKA depends on the measured level of the bicarbonate buffering system in the blood. DKA is “defined” as an elevated blood sugar level (300 mg/dL [16.7 mmol/L] or higher) with a lowered blood bicarbonate level (16 mmol/L or lower) plus evidence of dehydration. The buildup of acid in the bloodstream is indirectly measured by a calculation known as the “anion gap”. In DKA, the anion gap is greater than 12. The actual level of ketones in the blood does not define the presence of DKA, nor does the presence of nausea or vomiting.

Like with the blood sugar, the kidneys aim to pump out the ketones in the urine too. It is why urine ketone testing remains an important at home diabetes test. Blood ketone testing monitors have existed for over 15 years. Unfortunately, the kidneys can’t keep up with a massive ketone wave from low insulin levels and stress hormones. Enter the lungs.

The lungs have a special role in helping us to correct some acid-base imbalances. In addition to being acidic and dissolvable into water, some ketones are ‘aromatic’; capable of being excreted into the air. Exhaled air from persons with DKA contains acetone (the primary component of nail polish remover). Acetone has a light sweet fruity odor and can often be smelled by nearby observers. The patient usually can’t smell them and sometimes the family dismisses the odor. For the lungs to be able to maximally remove acetone, the rate and/or depth of breathing is usually increased. This special form of hyperventilation (a slow labored breathing) is called Kussmaul breathing by the doctor who first described the phenomenon long ago. Once the blood pH drops below 7.0 Kussmaul breathing tends to stop. That’s because the acid load is depressing the drive to breathe.

Another interesting adjustment the body makes is in minimizing the acid levels in the blood by trading the element potassium from inside cells for the acidic hydrogen which is part of any acid (like ketones). One molecule of potassium leaves a cell in exchange for 1 molecule of ketone acid. This serves to improve the pH of the blood but acts to deplete the cells of potassium too. Potassium is an essential element inside our cells. It is part of many vital chemical pathways which keep us healthy, including how signals pass in and out of cells, as well as how our nervous system works. Serious potassium (and sodium) deficiencies are part of DKA. Many major and minor electrolytes are washed out of the body in the urine tidal wave created by high blood sugars. Their proper replacement requires very careful attention and must be gradually replaced, usually intravenously.


Like water, potassium must be replaced carefully and with close supervision. Too much or too little potassium in the blood can cause muscular and nervous system malfunctions or even death due to cardiac arrest. Many other electrolytes are shifted in different directions during DKA. Once proper fluid and insulin therapy is started and carefully monitored during the recovery phase, these metabolic abnormalities will slowly correct. Insulin therapy drives potassium back into cells. A molecule of sugar takes a molecule of potassium inside the cell with it. Shifting potassium levels are closely watched during the initial treatment and recovery phase of DKA. Although the usual measures of DKA may improve in 24-48 hours, a full metabolic recovery from DKA may take days to weeks to occur.

The management of DKA revolves around careful rehydration, insulin therapy, and managing/preventing electrolyte abnormalities. Virtually every case of DKA has an element of dehydration present. Most patients get rehydrated gradually. Fluids given too fast or aggressively can be disastrous as discussed earlier. Gradual hydration is the best approach. This is often done in an intensive care setting in severe DKA cases.

Maintaining insulin therapy or increasing it as needed is an essential first step in preventing DKA. More than just insulin is needed. DKA can be slowed or prevented by effectively managing nausea (with at home anti-nausea medications) combined with careful and meticulous oral hydration. Frequent blood sugar and ketone checking are used to make decisions about when and how much to dose rapid-acting insulin.

Insulin may be dosed under close supervision as often as hourly by injection at home. Frequent blood sugar and ketone (blood or urine) checks help decide how often to dose insulin. Keeping up with ongoing water loss due to frequent urination is key to preventing further dehydration. Anti-nausea medications are helpful under close medical oversight. Frequent communication with the diabetes care team is very important.

Since DKA is also a state of dehydration, fluid therapy is the cornerstone of at home high blood sugar and ketone self-management. It’s helpful to take frequent sips of fluids rather than large gulps to reduce the likelihood of inducing vomiting.

When oral intake can’t happen due to frequent vomiting or persistent nausea, or if the person is impaired in any way, treatment must be promptly moved to an emergency room or hospital setting. If detected early enough, cases of early DKA can be prevented from becoming severe. Early recognition and detection of the pre-DKA state is extremely important.

If a parent or patient is not well trained in managing high sugars and ketones, then the best plan of action is a visit to an emergency department or urgent care clinic if blood sugars and ketone levels are both high. It might avert a possible admission or allow early treatment of a DKA case which could have been more severe had treatment been delayed further. Most importantly, don’t withhold scheduled insulin doses. Insulin omission opens the door to DKA. Typically, MORE insulin (amount and frequency) is needed.


Ketones can be measured in urine or blood at home. When using urine testing, any value rated as moderate or large, combined with a high blood sugar over 300 mg/dL (16.7 mmol/L) is worthy of careful attention. This means fluids and additional insulin as instructed by your doctor or diabetes team. If a home blood ketone meter is used, a blood ketone level more than 1.5 mmol/L plus BG over 300 mg/dL (16.7 mmol/L) is seen, then the risk of developing or being in DKA is high.


A very common mistake made by persons with known type 1 diabetes is to reduce or withhold insulin doses in response to most illnesses. Often this is done without carefully and more frequently checking blood sugars during an illness of any cause. The reasons for not checking sugars and insulin withholding are complex, but they are the most common oversights made. Insulin pump failures or malfunctions are a close second now that pump use is so prevalent. An insulin pump basal rate controls blood sugars for less than a few hours after it is interrupted by any type of pump malfunction. Skipping scheduled injections and failing to increase dosing to counteract stress or illness induced high blood sugars are common reasons for DKA.

The mental health or maturity of the person with diabetes cannot be ignored. Many children and teens are given the reigns of self-care too soon. The result is a lack of attention to details and more frequent self-care omissions, of which insulin dosing is extremely important. Not every insulin omission results in DKA. Therefore, some persons may become complacent and not believe insulin omission has serious consequences. This is a mistake of huge proportions.

Insulin omission (skipping one or more doses of scheduled insulin) caused my first episode of DKA when I was in college. At that time, I only took one daily injection of intermediate acting insulin (Lente). I ran out of insulin after my Saturday injection. Pharmacies were closed on Sundays in the town I lived in. I mistakenly thought I could just get insulin on Monday and everything would be alright. I didn’t have home blood sugar testing technology at that time. By Sunday afternoon I was feeling nauseous and tired. My first thought was to blame it on food poisoning from the hamburger I ate at lunch at the University cafeteria. After repeated vomiting mid-afternoon my roommate took me to the University infirmary. I was in DKA. It was the first time since my 1966 diagnosis (this was 1975). I had no idea what DKA was and sadly I was not taught anything about it afterwards.

Fast forward twenty years. I created the first Diabetes Sick Day video to educate parents and patients to prevent DKA from happening. I re-created it in 2003. Tens of thousands of people have seen it and it spawned many similar videos over the years. It’s something I am particularly proud of since I know it prevented DKA in many patients within and well beyond my practice. I often got backhanded complements from my pediatric resident trainees at the time. They complained that they were having a hard time learning how to manage DKA since we were keeping so many of them out of the hospital with diabetes sick day education. We made a commitment to ensure each patient or family got a free video, and that they reviewed it after a DKA admission to reduce the likelihood they would have another episode. We were pleased with the overall results.

The DKA video was eventually shown on a local cable TV so all could see anytime. Later it would be posted online. Here is the link:

DKA prevention education, combined with quick communication access to knowledgeable diabetes support staff or experienced on call endos 24/7/365 can keep DKA rates to a minimum. But education alone does not eliminate new cases of diabetes presenting as DKA. Too many cases go undiagnosed in doctor’s offices, urgent care facilities and emergency departments. I applaud groups which aim to improve the recognition of signs and symptoms of type 1 diabetes through greater professional and lay awareness. This effort must be an ongoing one as there will always be health care professionals with low levels of type 1 diabetes experience or knowledge.

It’s essential that every person with diabetes knows how to manage the pre-DKA state to steer it away from a full DKA event. Any insulin pump user will eventually experience a pump malfunction due to an improperly placed infusion site, a dislodged site, air bubbles or gaps in tubing, use of disintegrated insulin, improper loading of the reservoir, failure to prime the tubing, or mechanical defects in the pump itself. These often go unnoticed until the telltale signs of high blood sugar occur or the nausea and vomiting of a DKA event appears. If the person doesn’t attempt to check ketones (by blood or urine) and fails to aggressively manage the high blood sugars and stay properly hydrated, then DKA will quickly happen.

The state of the family has changed over my lifetime with diabetes. Divorce is more prevalent than 25 years ago. More kids with diabetes are living in different homes with varying amounts of diabetes self-care knowledge about DKA prevention. I see it more often during holidays when the child or teen spends time with the other ‘non-primary’ parent. The family may assume the child or teen is ready for independent management in part out of necessity. This puts a burden on the child or teen and increases DKA risk. If the divorced parents are not amicable, the poor communication further increases DKA risk. Blame is often placed by each parent on the other for the DKA admission. The child is typically caught in the middle. In some cases, I’ve seen the child or teen consciously omit insulin to get out of the home due to disagreements with the parents or a poor living arrangement. A DKA admission can sometimes serve as a teen’s temporary ticket out of a poor home situation. It can become part of a recurring pattern of DKA admissions.

Some parents may not realize or appreciate that DKA in a child or teen could be more than just lack of diabetes education. Latent diabetes anger or denial, depression, bipolar disorder, post-traumatic syndrome, bullying, even problems with gender identity can be some of the reasons why some children and teens repeatedly present to the hospital in DKA. Child abuse and neglect can also result in recurrent DKA. These must be considered when planning the care of a child or adult with type 1 diabetes.

I hope you have read to this point and have learned something you didn’t know at the beginning. Knowledge is power. Better choices and decisions are possible with the information above.

In closing, here are the answers to the six questions asked at the top of the post. Please remember these DKA and related myths and do your best to avoid perpetuating them:

MYTH: Overeating (carbs or anything else) causes DKA. THIS IS FALSE. This may raise blood sugars high, but it’s the absolute or relative lack of insulin which triggers the chemical cascade that can result in DKA if steps are not taken to interrupt its progression.

MYTH: Vomiting and nausea must be present in DKA. THIS IS FALSE. DKA can cause nausea and vomiting, but so can many other conditions or diseases. If acid levels in blood are too high, nausea may be present (but not always). Vomiting and nausea can also be symptoms of literally hundreds of other disorders or diseases. Just remember than whenever nausea and vomiting are present, there must be high vigilance for looking for DKA or the risk for impending DKA by checking blood sugars and ketone levels. But high sugar and ketones are going to be present in typical cases of DKA.

MYTH: Persons who are sick or stressed always need less insulin. THIS IS FALSE. In the DKA or pre-DKA state, MORE insulin is usually needed. The DKA state is one of absolute or relative insulin deficiency. The reasons are discussed above.

MYTH: All ketones are bad. THIS IS FALSE. Ketones per se are not bad actors! They are part of one’s normal metabolism, with or without diabetes. All healthy people make ketones, all day long. It’s a matter of how much and why. Learn when to react and when to not overreact to their presence.

MYTH: DKA only happens when I frequently omit scheduled insulin, use damaged insulin, or have an insulin pump malfunction. THIS IS FALSE. Many other situations can trigger DKA to occur, including a severe infection and certain medications like high dose steroids even when usual insulin doses are being taken.

MYTH: Insulin alone treats severe cases of DKA. THIS IS FALSE. DKA is a complex form of dehydration (intracellular) due to lack of sufficient insulin action. Dehydration and chemical imbalances (electrolytes) are commonplace. Careful fluid, insulin and electrolyte therapy are needed to effectively manage severe DKA.

The following are six tips to help prevent DKA


Never go to bed with ketones. Consistent fluid intake is needed to flush them out, along with frequent blood sugar checks and extra rapid-acting insulin as needed. If you or your child go to sleep with ketones still in your system, there is a very high probability they will not be gone by morning. They could even be higher.


When managing high blood sugar and ketones, rapid acting can be insulin can be given by injection as often as every hour. Check with your doctor or team of course. An hourly dose of rapid acting insulin (if dosed at a proper amount) can mimic the effect of an intravenous infusion of insulin of the same amount. One dose of insulin may not be enough to stop production of ketones and lower the high blood sugar level.


Good, timed and steady oral hydration with careful, measured administration of fluids is a cornerstone of ketone and high blood sugar at-home management. Strongly consider anti-nausea therapy as prescribed by your doctor to enhance chances of success.


Continued nausea and vomiting after a reasonable effort to treat should prompt immediate contact with the diabetes team or doctor. If ever in question, consider a trip to the emergency department or urgent care facility for more in depth evaluation.


Always check blood sugar 2 hours AFTER an insulin pump site change. It’s the best way to catch a faulty site insertion which can result in rapid onset DKA. Late evening site changes are the greatest risk for DKA by morning if the site is not placed properly and no follow up blood sugar check is performed.


Share the responsibility of insulin dosing with children and teens under 16. Insulin omission is the most common cause of DKA. Children and teens with diabetes who dose insulin with no oversight or supervision are much more likely to forget or omit a dose. This significantly raises the risk of developing DKA.

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