Diabetic ketoacidosis diet -
The treatment for DKA usually involves a combination of approaches to normalize blood sugar and insulin levels. Infection can increase the risk of DKA. If your DKA is a result of an infection or illness, your doctor will treat that as well, usually with antibiotics. At the hospital, your physician will likely give you intravenous IV fluids to help your body rehydrate.
During a DKA event, you usually lose a lot of fluids, which can reduce the amount of blood flowing through your body.
Fluid replacement helps restore typical blood flow. It also helps treat dehydration , which can cause even higher blood sugar levels.
Electrolytes are electrically charged minerals that help your body, including the heart and nerves, function properly. Electrolyte replacement is also commonly done through an IV. The emergency care team will also monitor several other blood test results that indicate when insulin therapy is no longer needed.
When your blood sugar and other test readings are within an acceptable range, your doctor will work with you to help you avoid DKA in the future. DKA occurs when insulin levels are low.
Our bodies need insulin to use the available glucose in the blood. Turning fat into energy produces ketones. When too many ketones build up, your blood becomes acidic. This is diabetic ketoacidosis. Although DKA is less common in people who have type 2 diabetes, it does occur.
A diagnosis of ketosis-prone diabetes is more likely for:. Testing for ketones is one of the first steps for diagnosing DKA. If you have type 1 diabetes, you should have a supply of home ketone tests. These test either your urine or your blood for the presence of ketones. According to the American Diabetes Association , you should test for ketones:.
Urine test strips change color to signal the presence of ketones in your urine. The indicator on the strip will change color. Compare the test strip to the results chart.
Blood ketone testers are also available. These are usually combination devices that can measure both glucose levels and ketone levels. The test strip is inserted into a monitor device to test for the presence of ketones in your blood.
A doctor will likely do a test to confirm the presence of ketones in your urine. They will usually also test your blood sugar level.
Other tests your doctor may order include:. There are many ways to prevent DKA. You can lower your risk of DKA with proper management of your diabetes:. Call your doctor if you detect moderate or high ketones in a home test. Early detection is essential.
Classification and diagnosis of diabetes: standards of care in diabetes Diabetes Care. PMID: pubmed. Maloney GE, Glauser JM. Diabetes mellitus and disorders of glucose homeostasis.
In: Walls RM, Hockberger RS, Gausche-Hill M, Erickson TB, Wilcox SR, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Updated by: Sandeep K. Dhaliwal, MD, board-certified in Diabetes, Endocrinology, and Metabolism, Springfield, VA. Also reviewed by David C. Dugdale, MD, Medical Director, Brenda Conaway, Editorial Director, and the A.
Editorial team. Diabetic ketoacidosis. DKA happens when the signal from insulin in the body is so low that: Blood sugar glucose can't go into cells to be used as a fuel source.
The liver makes a large amount of glucose. Fat is broken down too rapidly for the body to process. Common symptoms of DKA can include: Decreased alertness Deep, rapid breathing Dehydration Dry skin and mouth Flushed face Frequent urination or thirst that lasts for a day or more Fruity-smelling breath Headache Muscle stiffness or aches Nausea and vomiting Stomach pain.
Exams and Tests. Ketone testing is usually done when DKA is suspected: Most often, urine testing is done first.
If the urine is positive for ketones, most often a ketone called beta-hydroxybutyrate is measured in the blood. This is the most common ketone measured. The other main ketone is acetoacetate. Other tests for ketoacidosis include: Arterial blood gas Basic metabolic panel , a group of blood tests that measure your sodium and potassium levels, kidney function, and other chemicals and functions, including the anion gap Blood glucose test Blood pressure measurement Osmolality blood test.
Outlook Prognosis. Most people respond to treatment within 24 hours. Sometimes, it takes longer to recover. Importantly, these associations remained independent after adjusting for a number of factors including insulin dosing and physical activity.
While this observation may not go in line with the dietary recommendations, it has to be acknowledged that the results could also be a reflection of individuals prone to experience hypoglycaemia trying to prevent new episodes with higher carbohydrate intake in relation to that of fat.
The use of high carbohydrate, low fat diet to prevent hypoglycaemias could, however, be counterintuitive as a change from a standard diet to a low-carbohydrate diet rather has the potential to reduce the incidence of hypoglycaemias 13 , Importantly, while increased carbohydrate intake and the associated higher insulin doses give rise to larger variations in blood glucose concentrations 13 , 15 , marked reductions in glycaemic variability have been reported in studies of low-carbohydrate diets 14 , High variability of the blood glucose levels, on the other hand, is a well-known risk factor for hypoglycaemia 5 , 17 , a phenomenon that could also explain the current observations.
Fat intake, on the other hand, does not raise the blood glucose levels and, following the above reasoning and the current observations, would reduce the hypoglycaemia risk. Importantly, previous small studies have not identified differences in dietary intake in individuals with and without risk of severe hypoglycaemia 9 , Zhong et al.
suggested, however, that higher intakes of soluble fibre and protein were associated with daytime and nocturnal hypoglycaemia, while glycaemic index and the intakes of monounsaturated and polyunsaturated fatty acids were protective of daytime hypoglycaemia in adolescents with type 1 diabetes Overall, there is a shortage of large contemporary studies of the association between dietary intake and hypoglycaemia requiring hospitalisation in adults with type 1 diabetes such as the one presented in this paper.
Excessive alcohol intake is known to be associated with ketoacidosis. In a population of almost 30, young individuals with type 1 diabetes, for example, Hermann et al.
observed that the adjusted DKA rate was significantly increased in those with high alcohol intakes 6. In our study, even a small self-reported intake of alcohol measured either as absolute intake or as percentage of total energy intake, was associated with an increased risk of DKA.
This may reflect the relationship between self-reported alcohol intake and the frequency of binge drinking, although even small amounts of alcohol may affect hepatic metabolism Importantly, alcohol consumption may lead to reduced adherence to diabetes self-management practices and thereby increase the risk of acute complications.
Although recommendations of abstinence are often levelled at individuals at risk of hypoglycaemia, and alcohol consumption has been previously associated with hypoglycaemia 7 , in our study the major benefit of alcohol abstinence may be in those with poor glucose control at risk for DKA.
Beyond alcohol consumption, abundant intake of fibres intake was associated with reduced risk for DKA hospitalisation, in the current study. While we are not aware of prior studies showing such a protective effect, there is some indication that high fibre intake may be beneficial for blood glucose control 20 , 21 and, thus, could also impact the DKA risk.
A number of limitations are worthy of mention. As the study was observational and cross sectional data were collected only at one time point, it limits us from making causal inferences.
While the role of alcohol consumption in the risk of DKA is fairly well established, our observations linking high carbohydrate and low fat intake to severe hypoglycaemia may also be explained by a reverse causation. It should also be noted that the dietary intake was self-reported. Importantly, data collected with self-report methods may be subject to misreporting.
Whether individuals prone to develop severe hypoglycaemia or DKA would systematically differ in misreporting from those in low risk is however not known. Importantly, individuals with and without hospitalisations were comparable with respect to many background variables, including socioeconomic status, depressive symptomatology, and physical activity.
Dietary intake was also only reported at one point, in the middle of the 4-year observation period for the hospitalizations. In a small sample of individuals with diet recording repeated within a 4-year time frame, however, we observed no difference in energy, fibre, or macronutrient intake, suggesting that during the selected two-sided 2-year time period no major changes in dietary intake took place.
It should also be noted that data on a number of important confounders, including hypoglycaemia awareness, family support, and type of insulin used, were not available for the analyses. In the current study, DKA and severe hypoglycaemia were identified from hospitalisation registries. With the use of such registries we were able to reliably identify all severe cases that needed acute inpatient care.
However with this method we likely missed a number of milder cases that were treated in outpatient units or by friends and family members, and therefore reduced power to identify associations between dietary exposures and acute complications.
Finally, as the study participants were volunteers, individuals less interested in diet and health-related matters may have been under-represented in this sample. The potential under-representation of individuals with less healthy life-styles and dietary practices would likely have diluted the phenomenon taking place in the real-world.
With these limitations in mind, the current study with a large number of well-defined individuals with type 1 diabetes is an important addition to the limited pool of knowledge on the association between dietary intake and acute complications of type 1 diabetes.
In conclusion, supported by the current dietary guidelines, alcohol intake was associated with an increased DKA admission risk, and abundant intake of fibres rather reduced the risk. Increasing carbohydrate intake at the expense of fat, instead, was associated with increased risk of hypoglycaemia hospitalisations.
More studies are needed to reveal the associations between diet and acute complications of type 1 diabetes. Participants were individuals with type 1 diabetes taking part in the ongoing nation-wide Finnish Diabetic Nephropathy FinnDiane Study.
In the FinnDiane Study, included are individuals with the onset of diabetes prior to the age of 40 years and permanent insulin treatment initiated within a year from the diabetes diagnosis. In the current analyses, all adult FinnDiane Study participants, investigated between August and January , with a completed food record as described in more detail below, were included.
The study was carried out in accordance with the Declaration of Helsinki and its later amendments. All participants signed written informed consent prior to study participation.
Cross-sectional data from individuals participating in the FinnDiane study, in whom records of dietary intake, data on smoking habits, alcohol intake, insulin dosing, physical activity, and social class, using a self-reported patient questionnaire, were included.
The reported insulin dose was divided by weight in kg. Based on the reported duration and intensity of physical activity, metabolic equivalent of task hours METh was calculated for each participant. Unskilled blue collar workers were classified as having low socioeconomic status.
Depression was assessed using Beck Depression Inventory BDI 22 , as previously described Details on clinical status, including age at diagnosis, insulin therapy and other regular medications, together with presence, severity and management of diabetic complications including diabetic retinopathy and macrovascular disease, were obtained from medical records by the attending physician using a standardised questionnaire.
Blood pressure measurements were performed twice in the sitting position, with a ten-minute interval between testing, with the mean of the two measurements was calculated.
Fasting blood samples were obtained for the measurement of HbA 1c , lipids and creatinine, assayed at the laboratory of the Helsinki University Hospital. HbA 1c was assessed locally using a standardized assay. The glomerular filtration rate GFR was estimated using the CKD-EPI formula The methods to study dietary intake, in the FinnDiane Study, have been previously described in more detail The study visit took place at around the same time as the diet assessment.
The dates for these 3 days were allocated and covered consecutive days either from Thursday to Saturday or Sunday to Tuesday.
In order to capture variation in the dietary intake, the other set of days Sunday to Tuesday or Thursday to Saturday, respectively was allocated for the second recording.
For the purpose of the current study, data collected with the diet records were only used. AivoDiet software version 2. For the analyses, we only included participants with plausible energy intake 5.
To test the repeatability of the diet recording over the years, we additionally identified individuals with two diet recordings within a 4 year time window. Data on DKA and hypoglycaemia hospitalisations, for the above mentioned FinnDiane Study participants, were obtained from the Finnish nation-wide health registries.
Only events that occurred in a four-year window, two years prior and two years after the formal assessment of the dietary intake are reported in this study.
Data on categorical variables are presented as frequencies, while continuous variables with skewed distribution are shown as medians interquartile ranges.
Between-group comparisons were performed with Chi-squared test and Mann—Whitney U-test, respectively. In addition, we applied macronutrient substitution where one macronutrient at a time was excluded from the model.
In the models, we included age, sex, insulin dosing, physical activity, and total energy intake for both endpoints. For the purpose of studying the repeatability of the diet records, we used paired samples t-test.
Analyses were done using IBM SPSS Statistics for Windows, Version Kristensen, P. et al. Insulin analogues and severe hypoglycaemia in type 1 diabetes. Diabetes Res. Article CAS Google Scholar.
International Hypoglycaemia Study Group. Hypoglycaemia, cardiovascular disease, and mortality in diabetes: Epidemiology, pathogenesis, and management. Lancet Diabetes Endocrinol. Article Google Scholar. Weinert, L. Precipitating factors of diabetic ketoacidosis at a public hospital in a middle-income country.
Morris, A. Adherence to insulin treatment, glycaemic control, and ketoacidosis in insulin-dependent diabetes mellitus. Diabetes Audit and Research in Tayside Scotland. Medicines Monitoring Unit. Lancet , — Malkani, S. Frequency and predictors of self-reported hypoglycemia in insulin-treated diabetes.
Hermann, J. Self-reported regular alcohol consumption in adolescents and emerging adults with type 1 diabetes: A neglected risk factor for diabetic ketoacidosis? Multicenter analysis of 29 patients from the DPV registry. Diabetes 18 , — Tetzschner, R. Effects of alcohol on plasma glucose and prevention of alcohol-induced hypoglycemia in type 1 diabetes—A systematic review with GRADE.
Diabetes Metab. Cooper, H. Risk factors for recurrent admissions with diabetic ketoacidosis: A case-control observational study.
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